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Original Article
Basic and Translational Research
Article image
Targeting PGC-1α by miRNA-374 Simultaneously Improve β-Cell Dysfunction and Suppress Hepatic Glucose Overproduction
Ji-Won Kim, Joonyub Lee, Young-Hye You, Chan-Hee Oh, Heon-Seok Park, Eun Young Lee, Seung-Hwan Lee, Seung-Hyun Ko, Ji-Ho Park, Kun-Ho Yoon
Received April 5, 2025  Accepted August 24, 2025  Published online November 3, 2025  
DOI: https://doi.org/10.4093/dmj.2025.0287    [Epub ahead of print]
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AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
In this study, we aimed to validate the potential of miR-374 in ameliorating hyperglycemia by regulating peroxisome proliferator-activated receptor γ coactivator-1 (PGC-1α) expression in pancreatic islets and liver.
Methods
To identify miRNAs targeting PGC-1α, we performed miRNA chip analysis in rat islets under hyperglycemic and euglycemic conditions. Luciferase reporter assay was performed to identify miR binding sites in the 3’-untranslated region (3’ UTR) of PGC-1α. In db/db mice, miRNA-encapsulated adenoviruses were administered and intraperitoneal glucose tolerance test and glucose stimulated insulin secretion tests were performed. For enhanced delivery to β-cells, we developed exendin-4 (Ex-4) coated cationic lipoparticles (CCLs) encapsulating miRNAs. The therapeutic potential of Ex-4-CCL-miRNA was further evaluated in insulin-producing cells derived from induced pluripotent stem cells.
Results
By analyzing miRNA expression in primary rat islets exposed under hyperglycemic environment, we identified miR-374 as a potential target. In vitro experiments confirmed that miR-374 significantly suppressed PGC-1α expression in β-cells and hepatocytes by binding to its 3’-UTR. In vivo experiments using adenovirus-mediated miR-374 (Ad-miR-374) delivering directly to the pancreas and liver of db/db mice demonstrated improved glycemic control, enhanced insulin secretion, and downregulated hepatic gluconeogenesis-related genes (G6Pase, Pepck, PC). To enhance the clinical applicability of miR-374, we developed Ex-4-CCLs. Ex-4-CCL-miR-374 successfully alleviated hyperglycemia, restored pancreatic islet function, and decreased gluconeogenesis gene expression in db/db mice. Furthermore, Ex-4-CCL-miR-374 improved insulin secretory function in glucotoxicity-exposed human induced pluripotent stem cell-derived insulin producing cells.
Conclusion
Based on these findings, we propose that Ex-4-CCL-miR-374 as a promising therapeutic approach to reverse β-cell dysfunction and improve hepatic insulin resistance in type 2 diabetes mellitus.

Citations

Citations to this article as recorded by  
  • β‐cell recovery revisited: Is prediabetes remission driven by insulin sensitivity or β‐cell function?
    Joonyub Lee, Kun‐Ho Yoon
    Journal of Diabetes Investigation.2026;[Epub]     CrossRef
Review
Guideline/Statement/Fact Sheet
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Defining Severe Diabetes Mellitus: A Consensus Framework for Grading and Staging Diabetes Based on Pathophysiology and Complications
Jae Hyun Bae, Hun Jee Choe, Ye Seul Yang, Mi Hae Seo, Jong Han Choi, Gyuri Kim, Young Sang Lyu, Jeung Hun Han, Shinae Kang, Won Jun Kim, Kyung-Soo Kim, Young Min Cho, Bong Soo Cha, for the Severe Diabetes Mellitus Task Force of the Korean Diabetes Association
Diabetes Metab J. 2025;49(6):1141-1154.   Published online October 28, 2025
DOI: https://doi.org/10.4093/dmj.2025.0739
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AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Diabetes mellitus comprises a heterogeneous group of metabolic disorders differing in etiology, clinical course, and outcomes. Traditional classifications, such as type 1 and type 2 diabetes mellitus, fail to capture the full heterogeneity, including variation in insulin deficiency, insulin resistance, and complication burden. To address these limitations, we propose the Diabetes Grade–Stage Classification, an integrated system that combines pathophysiology-based grading with complication-based staging. Grading quantifies metabolic dysfunction through the assessment of insulin deficiency and insulin resistance. In parallel, staging assesses the extent of target organ damage, particularly in the cardiovascular, renal, ocular, and nervous systems. Together, this framework enables a comprehensive assessment of disease status, identification of vulnerable or high-risk phenotypes, and implementation of risk-adapted management strategies. Clinically, it facilitates personalized care, promotes collaborative coordination, and strengthens physician–patient communication. Furthermore, this framework provides a scalable structure for integrating disease severity into both individual- and population-level interventions. Although the current criteria for grading and staging are based on expert consensus and selected clinical indicators, such as low C-peptide levels and advanced complications, further validation and refinement are needed. In conclusion, the grading and staging system provides an operational tool for classifying the severity of diabetes mellitus and has the potential to extend life expectancy and improve quality of life for people living with diabetes mellitus.

Citations

Citations to this article as recorded by  
  • Bridging Evidence and Practice: A Consensus Statement from the Korean Diabetes Association on Diabetes Screening, Pharmacological Treatment and Severe Diabetes
    Jong Han Choi, Shinae Kang, Soo-Kyung Kim, Won Jun Kim, Ji Min Kim, Jaehyun Bae, Jae-Seung Yun, Eonju Jeon, Young-Eun Kim, Jae Hyun Bae, Hun Jee Choe, Young Min Cho, Seung-Hyun Ko, Sang Yong Kim, Hae Jin Kim, You-Cheol Hwang, Min Kyong Moon, Suk Chon, Seo
    Diabetes & Metabolism Journal.2025; 49(6): 1155.     CrossRef
Original Articles
Metabolic Risk/Epidemiology
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Beta-Cell Function, Insulin Sensitivity, and Metabolic Characteristics in Young-Onset Type 2 Diabetes Mellitus: Findings from Anam Diabetes Observational Study
Ji Yoon Kim, Jiyoon Lee, Sin Gon Kim, Nam Hoon Kim
Diabetes Metab J. 2025;49(6):1287-1297.   Published online May 21, 2025
DOI: https://doi.org/10.4093/dmj.2024.0601
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AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
In this study, we aimed to determine the metabolic characteristics and changes in the early stages of young-onset type 2 diabetes mellitus (YOD) in Koreans.
Methods
From the Anam Diabetes Observational Study cohort (2017–2023), the characteristics of newly diagnosed YOD (<40 years of age, n=39) and later-onset (≥40 years of age) type 2 diabetes mellitus (LOD, n=178) were compared at diagnosis and 1 year later. All participants underwent an oral glucose tolerance test at diagnosis and annually thereafter. β-Cell function was determined using the disposition index (DI), calculated as the insulinogenic index×Matsuda insulin sensitivity index (ISI). Insulin sensitivity was determined using ISI and homeostasis model assessment of insulin resistance (HOMA2-IR).
Results
Mean (±standard deviation) age of individuals with YOD was 29.8±6.4 years, and 76.9% were male. YOD patients had higher body mass index (29.8 kg/m2 vs. 27.2 kg/m2, P=0.020), fat mass (30.5 kg vs. 24.1 kg, P=0.011), fatty liver index (65.4 vs. 49.2, P=0.005), and glycosylated hemoglobin (HbA1c) level at diagnosis (9.3% vs. 7.7%, P<0.001) compared with LOD patients. YOD patients exhibited lower insulin sensitivity (ISI: 2.79 vs. 3.26, P=0.008; HOMA2-IR: 2.72 vs. 1.83, P<0.001) and β-cell function (DI) at diagnosis (0.41 vs. 0.72, P=0.003) than LOD patients. Following 1 year of treatment, DI improved by 94% in YOD along with improvement in HbA1c; however, it was still significantly lower than that of LOD (0.64 vs. 0.90, P=0.017).
Conclusion
Individuals with YOD have unfavorable metabolic characteristics, substantially reduced insulin sensitivity, and decompensated β-cell function at disease onset, which persist even after treatment.
Others
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Contributions of Hepatic Insulin Resistance and Islet β-Cell Dysfunction to the Blood Glucose Spectrum in Newly Diagnosed Type 2 Diabetes Mellitus
Mengge Yang, Ying Wei, Jia Liu, Ying Wang, Guang Wang
Diabetes Metab J. 2025;49(4):883-892.   Published online February 13, 2025
DOI: https://doi.org/10.4093/dmj.2024.0537
Correction in: Diabetes Metab J 2026;50(2):432
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AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Our previous studies have investigated the role of hepatic insulin resistance (hepatic IR) and islet β-cell function in the pathogenesis of diabetes. This study aimed to explore the contributions of hepatic IR and islet β-cell dysfunction to the blood glucose spectrum in patients with newly diagnosed type 2 diabetes mellitus.
Methods
Hepatic IR was assessed by the hepatic insulin resistance index (HIRI). Islet β-cell function was assessed by insulin secretion- sensitivity index-2 (ISSI2). The associations between blood glucose spectrum and hepatic IR and ISSI2 were analyzed.
Results
A total of 707 patients with new-onset diabetes were included. The fasting blood glucose (FBG) and 30 minutes postload blood glucose elevated with rising HIRI (both P for trend <0.001). The FBG, 30 minutes, 2 hours, and 3 hours post-load blood glucose elevated with decreasing ISSI2 quartiles (all P for trend <0.001). There was a negative correlation between ISSI2 and HIRI after adjusting blood glucose levels (r=–0.199, P<0.001).
Conclusion
Hepatic IR mainly contributed to FBG and early-phase postprandial plasma glucose, whereas β-cell dysfunction contributed to fasting and postprandial plasma glucose at each phase.

Citations

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  • Interaction between insulin resistance and depression in predicting cardiovascular risk: Evidence from a longitudinal study
    Siyu Chen, Lijing Yang, Yu Zhou, Hao Yu
    Diabetes & Vascular Disease Research.2026;[Epub]     CrossRef
  • Engineering the pancreatic niche: Mechanobiological insights into stem cell-derived β-cell therapy for diabetes mellitus
    Swaminadhan Dandapani, Yongsung Hwang
    Mechanobiology.2026;[Epub]     CrossRef
  • Associations of adipose tissue insulin resistance with fasting blood glucose and HbA1c in adults without diabetes
    Ying Wei, Yong Tian, Ruixiang Cui, Ying Wang, Jia Liu, Guang Wang
    Diabetes, Obesity and Metabolism.2026; 28(4): 3209.     CrossRef
  • Advancing in vitro vascular wall modelling using digital light processing to study hyperglycemia-driven cell changes
    Ianina Pokholenko, Marguerite Meeremans, Sandra Van Vlierberghe, Nele Pien, Catharina De Schauwer
    Frontiers in Bioengineering and Biotechnology.2026;[Epub]     CrossRef
  • Redefining β-Cell Function in Type 2 Diabetes Mellitus: From Comprehensive Assessment to Precision Medicine
    YongKyung Kim, Joon Ha, Jun Sung Moon
    Diabetes & Metabolism Journal.2026; 50(2): 235.     CrossRef
  • Molecular epidemiology of the MTHFR C677T polymorphism and its association with type 2 diabetes mellitus at the University of Gondar Comprehensive Specialized Hospital
    Genetu Kassahun Berie, Mequanente Dagnaw, Meera Indracanti, Muluken Dejen, Nega Berhane
    Annals of Human Biology.2026;[Epub]     CrossRef
  • GLDC attenuates liver ischemia-reperfusion injury by inhibiting macrophage recruitment and activation via PTBP1/P2RY6
    Zhitao Li, Li Jin, Yuan Fang, Siming Qu, Bo Yuan, Kai Gan, Hanfei Huang
    Cellular Signalling.2025; 135: 111976.     CrossRef
  • The Physiological and Pathological Mechanisms of LIN2, LIN7, LIN10 and Their Tripartite Complex
    Yangyang Shang, Xinyi Gan, Yue Dang, Jie Liu, Peijun Liu
    Journal of Cellular and Molecular Medicine.2025;[Epub]     CrossRef
  • Cinnamic Acid: A Shield Against High-Fat-Diet-Induced Liver Injury—Exploring Nrf2’s Protective Mechanisms
    Asmahan Taher Alahdal, Laila Naif Al-Harbi, Ghedeir M. Alshammari, Ali Saleh, Mohammed Abdo Yahya
    International Journal of Molecular Sciences.2025; 26(16): 7940.     CrossRef
  • Sodium Butyrate Ameliorated Bile Acid Metabolism in Diabetes Mellitus by PI3K/AKT Signaling Pathway via the Gut–Liver Axis
    Tingting Zhao, Xi Zhang, Qian Xiang, Yadi Liu, Xuling Li, Junling Gu, Wenqian Zhang, Zhe Wang, Yiran Li, Xiaoshan Lai, Yonghua Zhao, Youhua Xu
    Current Issues in Molecular Biology.2025; 47(9): 732.     CrossRef
  • Chronic Intermittent Low-Pressure Hypoxia Suppresses Inflammation and Regulates Glycolipids by Modulating Mitochondrial Respiration in db/db Mice
    Xin Jiang, Keqing Yuan, Xiaofeng Ge, Lili Yu, Yufei Cui, Lianhai Jin, Ying Chang
    Metabolites.2025; 15(11): 707.     CrossRef
  • Expanding horizons: the role of robotic surgery in modern transplantation practices
    Arya Afrooghe, Pedram Pirmoradian, Moein Ghasemi, Benyamin Mohammadi, Mahya Soleymani Mehranjani, Elham Ahmadi, Seyed Amir Miratashi Yazdi
    Journal of Robotic Surgery.2025;[Epub]     CrossRef
  • Elevated PEDF promotes the occurrence of diabetes mellitus via suppressing GSIS by downregulating the SNARE complex
    Zhen Zhao, Yandan Tan, Jie Fang, Gan Xia, Junchen Li, Qilong Tang, Wanting Xie, Tianxiao Gao, Zhenzhen Fang, Ti Zhou, Xia Yang, Guoquan Gao, Weiwei Qi
    Communications Biology.2025;[Epub]     CrossRef
  • Distinct Circulating Biomarker Profiles Associated with Type 2 Diabetes in a Regional Cohort—A Cross-Sectional Study
    Abdullah Alsrhani, Muhammad Atif, Aisha Farhana
    Metabolites.2025; 15(12): 776.     CrossRef
  • Application and Predictive Potential of Novel Insulin Resistance Assessment Indices in Metabolic Diseases
    莹莹 郑
    Advances in Clinical Medicine.2025; 15(12): 2174.     CrossRef
Pathophysiology
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Recent Glycemia Is a Major Determinant of β-Cell Function in Type 2 Diabetes Mellitus
Ji Yoon Kim, Jiyoon Lee, Sin Gon Kim, Nam Hoon Kim
Diabetes Metab J. 2024;48(6):1135-1146.   Published online June 17, 2024
DOI: https://doi.org/10.4093/dmj.2023.0359
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  • 6 Web of Science
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AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Progressive deterioration of β-cell function is a characteristic of type 2 diabetes mellitus (T2DM). We aimed to investigate the relative contributions of clinical factors to β-cell function in T2DM.
Methods
In a T2DM cohort of 470 adults (disease duration 0 to 41 years), β-cell function was estimated using insulinogenic index (IGI), disposition index (DI), oral disposition index (DIO), and homeostasis model assessment of β-cell function (HOMA-B) derived from a 75 g oral glucose tolerance test (OGTT). The relative contributions of age, sex, disease duration, body mass index, glycosylated hemoglobin (HbA1c) levels (at the time of the OGTT), area under the curve of HbA1c over time (HbA1c AUC), coefficient of variation in HbA1c (HbA1c CV), and antidiabetic agents use were compared by standardized regression coefficients. Longitudinal analyses of these indices were also performed.
Results
IGI, DI, DIO, and HOMA-B declined over time (P<0.001 for all). Notably, HbA1c was the most significant factor affecting IGI, DI, DIO, and HOMA-B in the multivariable regression analysis. Compared with HbA1c ≥9%, DI was 1.9-, 2.5-, 3.7-, and 5.5-fold higher in HbA1c of 8%–<9%, 7%–<8%, 6%–<7%, and <6%, respectively, after adjusting for confounding factors (P<0.001). Conversely, β-cell function was not affected by the type or duration of antidiabetic agents, HbA1c AUC, or HbA1c CV. The trajectories of the IGI, DI, DIO, and HOMA-B mirrored those of HbA1c.
Conclusion
β-Cell function declines over time; however, it is flexible, being largely affected by recent glycemia in T2DM.

Citations

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  • An interpretable machine learning model for predicting metabolic dysfunction‐associated steatotic liver disease in patients with type 2 diabetes
    Zhuolin Zhou, Nan Gao, Jiaojiao Liu, Xuerong Ma, Zhijuan Ge, Cheng Ji
    Diabetes, Obesity and Metabolism.2026; 28(1): 122.     CrossRef
  • Machine learning and engagement insights for personalized blood glucose management
    Inbar Breuer Asher, David L. Horwitz, Omar Manejwala, Yifat Fundoiano-Hershcovitz
    Frontiers in Digital Health.2026;[Epub]     CrossRef
  • Redefining β-Cell Function in Type 2 Diabetes Mellitus: From Comprehensive Assessment to Precision Medicine
    YongKyung Kim, Joon Ha, Jun Sung Moon
    Diabetes & Metabolism Journal.2026; 50(2): 235.     CrossRef
  • Synergistic benefit of thiazolidinedione and sodium-glucose cotransporter 2 inhibitor for metabolic dysfunction-associated steatotic liver disease in type 2 diabetes: a 24-week, open-label, randomized controlled trial
    Minyoung Lee, Sukchul Hong, Yongin Cho, Hyungjin Rhee, Min Heui Yu, Jaehyun Bae, Yong-ho Lee, Byung-Wan Lee, Eun Seok Kang, Bong-Soo Cha
    BMC Medicine.2025;[Epub]     CrossRef
  • Beta-Cell Function, Insulin Sensitivity, and Metabolic Characteristics in Young-Onset Type 2 Diabetes Mellitus: Findings from Anam Diabetes Observational Study
    Ji Yoon Kim, Jiyoon Lee, Sin Gon Kim, Nam Hoon Kim
    Diabetes & Metabolism Journal.2025; 49(6): 1287.     CrossRef
  • Unlocking Gut-Driven Metabolic Repair: The Role of Glucomannan Porang (Amorphophallus muelleri Blume) in Insulin Resistance and Short-Chain Fatty Acid Modulation in a Type 2 Diabetes Mellitus Rat Model
    Azizah H. Safitri, Rahmata A. Sayyida, Eni Widayati, Nurina Tyagita
    Tropical Journal of Natural Product Research.2025;[Epub]     CrossRef
  • The Importance of Treating Hyperglycemia in β-Cell Dysfunction of Type 2 Diabetes Mellitus
    Arim Choi, Kyung-Soo Kim
    Diabetes & Metabolism Journal.2024; 48(6): 1056.     CrossRef
Metabolic Risk/Epidemiology
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A Prospective 1-Year Follow-up of Glycemic Status and C-Peptide Levels of COVID-19 Survivors with Dysglycemia in Acute COVID-19 Infection
David Tak Wai Lui, Chi Ho Lee, Ying Wong, Carol Ho Yi Fong, Kimberly Hang Tsoi, Yu Cho Woo, Kathryn Choon Beng Tan
Diabetes Metab J. 2024;48(4):763-770.   Published online March 11, 2024
DOI: https://doi.org/10.4093/dmj.2023.0175
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AbstractAbstract PDFPubReader   ePub   
Background
We evaluated changes in glycemic status, over 1 year, of coronavirus disease 2019 (COVID-19) survivors with dysglycemia in acute COVID-19.
Methods
COVID-19 survivors who had dysglycemia (defined by glycosylated hemoglobin [HbA1c] 5.7% to 6.4% or random glucose ≥10.0 mmol/L) in acute COVID-19 were recruited from a major COVID-19 treatment center from September to October 2020. Matched non-COVID controls were recruited from community. The 75-g oral glucose tolerance test (OGTT) were performed at baseline (6 weeks after acute COVID-19) and 1 year after acute COVID-19, with HbA1c, insulin and C-peptide measurements. Progression in glycemic status was defined by progression from normoglycemia to prediabetes/diabetes, or prediabetes to diabetes.
Results
Fifty-two COVID-19 survivors were recruited. Compared with non-COVID controls, they had higher C-peptide (P< 0.001) and trend towards higher homeostasis model assessment of insulin resistance (P=0.065). Forty-three COVID-19 survivors attended 1-year reassessment. HbA1c increased from 5.5%±0.3% to 5.7%±0.2% (P<0.001), with increases in glucose on OGTT at fasting (P=0.089), 30-minute (P=0.126), 1-hour (P=0.014), and 2-hour (P=0.165). At baseline, 19 subjects had normoglycemia, 23 had prediabetes, and one had diabetes. Over 1 year, 10 subjects (23.8%; of 42 non-diabetes subjects at baseline) had progression in glycemic status. C-peptide levels remained unchanged (P=0.835). Matsuda index decreased (P=0.007) and there was a trend of body mass index increase from 24.4±2.7 kg/m2 to 25.6±5.2 (P=0.083). Subjects with progression in glycemic status had more severe COVID-19 illness than non-progressors (P=0.030). Reassessment was not performed in the control group.
Conclusion
Subjects who had dysglycemia in acute COVID-19 were characterized by insulin resistance. Over 1 year, a quarter had progression in glycemic status, especially those with more severe COVID-19. Importantly, there was no significant deterioration in insulin secretory capacity.

Citations

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  • Reduced IFN-γ-expressing SARS-CoV-2 specific CD4+ T cells and transient CD8 + T cell activation associate with higher HOMA-IR 1-year post COVID-19 in obese individuals
    Rona Kartika, Dicky Levenus Tahapary, Farid Kurniawan, Syahidatul Wafa, Tika Pradnjaparamita, Simon P. Jochems, Heri Wibowo, Imam Subekti
    Scientific Reports.2025;[Epub]     CrossRef
Review
Pathophysiology
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Endoplasmic Reticulum Stress and Dysregulated Autophagy in Human Pancreatic Beta Cells
Seoil Moon, Hye Seung Jung
Diabetes Metab J. 2022;46(4):533-542.   Published online July 27, 2022
DOI: https://doi.org/10.4093/dmj.2022.0070
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  • 23 Web of Science
  • 24 Crossref
AbstractAbstract PDFPubReader   ePub   
Pancreatic beta cell homeostasis is crucial for the synthesis and secretion of insulin; disruption of homeostasis causes diabetes, and is a treatment target. Adaptation to endoplasmic reticulum (ER) stress through the unfolded protein response (UPR) and adequate regulation of autophagy, which are closely linked, play essential roles in this homeostasis. In diabetes, the UPR and autophagy are dysregulated, which leads to beta cell failure and death. Various studies have explored methods to preserve pancreatic beta cell function and mass by relieving ER stress and regulating autophagic activity. To promote clinical translation of these research results to potential therapeutics for diabetes, we summarize the current knowledge on ER stress and autophagy in human insulin-secreting cells.

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    Giorgio Vivacqua, Romina Mancinelli, Stefano Leone, Rosa Vaccaro, Ludovica Garro, Simone Carotti, Ludovica Ceci, Paolo Onori, Luigi Pannarale, Antonio Franchitto, Eugenio Gaudio, Arianna Casini
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    Min Jeong Park, Kyung Mook Choi
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    Kun Cui, Zhizheng Li
    Frontiers in Endocrinology.2023;[Epub]     CrossRef
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    Xiaodan Zhang, Zirui Luo, Jiahong Li, Yaxuan Lin, Yu Li, Wangen Li
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    Asie Sadeghi, Maryam Niknam, Mohammad Amin Momeni-Moghaddam, Maryam Shabani, Hamid Aria, Alireza Bastin, Maryam Teimouri, Reza Meshkani, Hamed Akbari
    European Journal of Medical Research.2023;[Epub]     CrossRef
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    Patricia Thomas, Meurig T. Gallagher, Gabriela Da Silva Xavier
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Original Article
Basic Research
DA-1241, a Novel GPR119 Agonist, Improves Hyperglycaemia by Inhibiting Hepatic Gluconeogenesis and Enhancing Insulin Secretion in Diabetic Mice
Youjin Kim, Si Woo Lee, Hyejin Wang, Ryeong-Hyeon Kim, Hyun Ki Park, Hangkyu Lee, Eun Seok Kang
Diabetes Metab J. 2022;46(2):337-348.   Published online January 21, 2022
DOI: https://doi.org/10.4093/dmj.2021.0056
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  • 19 Web of Science
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AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
We investigated the antidiabetic effects of DA-1241, a novel G protein-coupled receptor (GPR) 119 agonist, in vitro and in vivo.
Methods
DA-1241 was administrated to high-fat diet (HFD)-fed C57BL/6J mice for 12 weeks after hyperglycaemia developed. Oral/intraperitoneal glucose tolerance test and insulin tolerance test were performed. Serum insulin and glucagon-like peptide-1 (GLP-1) levels were measured during oral glucose tolerance test. Insulinoma cell line (INS-1E) cells and mouse islets were used to find whether DA-1241 directly stimulate insulin secretion in beta cell. HepG2 cells were used to evaluate the gluconeogenesis and autophagic process. Autophagic flux was evaluated by transfecting microtubule-associated protein 1 light chain 3-fused to green fluorescent protein and monomeric red fluorescent (mRFP-GFP-LC3) expression vector to HepG2 cells.
Results
Although DA-1241 treatment did not affect body weight gain and amount of food intake, fasting blood glucose level decreased along with increase in GLP-1 level. DA-1241 improved only oral glucose tolerance test and showed no effect in intraperitoneal glucose tolerance test. No significant effect was observed in insulin tolerance test. DA-1241 did not increase insulin secretion in INS-1E cell and mouse islets. DA-1241 reduced triglyceride content in the liver thereby improved fatty liver. Additionally, DA-1241 reduced gluconeogenic enzyme expression in HepG2 cells and mouse liver. DA-1241 reduced autophagic flow in HepG2 cells.
Conclusion
These findings suggested that DA-1241 augmented glucose-dependent insulin release via stimulation of GLP-1 secretion, and reduced hepatic gluconeogenesis, which might be associated with autophagic blockage, leading to improved glycaemic control.

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Review
Technology/Device
Article image
Assessment of Insulin Secretion and Insulin Resistance in Human
So Young Park, Jean-François Gautier, Suk Chon
Diabetes Metab J. 2021;45(5):641-654.   Published online September 30, 2021
DOI: https://doi.org/10.4093/dmj.2021.0220
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  • 1,625 Download
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Graphical AbstractGraphical Abstract AbstractAbstract PDFPubReader   ePub   
The impaired insulin secretion and increased insulin resistance (or decreased insulin sensitivity) play a major role in the pathogenesis of all types of diabetes mellitus (DM). It is very important to assess the pancreatic β-cell function and insulin resistance/ sensitivity to determine the type of DM and to plan an optimal management and prevention strategy for DM. So far, various methods and indices have been developed to assess the β-cell function and insulin resistance/sensitivity based on static, dynamic test and calculation of their results. In fact, since the metabolism of glucose and insulin is made through a complex process related with various stimuli in several tissues, it is difficult to fully reflect the real physiology. In order to solve the theoretical and practical difficulties, research on new index is still in progress. Also, it is important to select the appropriate method and index for the purpose of use and clinical situation. This review summarized a variety of traditional methods and indices to evaluate pancreatic β-cell function and insulin resistance/sensitivity and introduced novel indices.

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Original Articles
Basic Research
Article image
Notch1 Has an Important Role in β-Cell Mass Determination and Development of Diabetes
Young Sil Eom, A-Ryeong Gwon, Kyung Min Kwak, Jin-Young Youn, Heekyoung Park, Kwang-Won Kim, Byung-Joon Kim
Diabetes Metab J. 2021;45(1):86-96.   Published online February 26, 2020
DOI: https://doi.org/10.4093/dmj.2019.0160
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Graphical AbstractGraphical Abstract AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background

Notch signaling pathway plays an important role in regulating pancreatic endocrine and exocrine cell fate during pancreas development. Notch signaling is also expressed in adult pancreas. There are few studies on the effect of Notch on adult pancreas. Here, we investigated the role of Notch in islet mass and glucose homeostasis in adult pancreas using Notch1 antisense transgenic (NAS).

 Methods

Western blot analysis was performed for the liver of 8-week-old male NAS mice. We also conducted an intraperitoneal glucose tolerance test (IPGTT) and intraperitoneal insulin tolerance test in 8-week-old male NAS mice and male C57BL/6 mice (control). Morphologic observation of pancreatic islet and β-cell was conducted in two groups. Insulin secretion capacity in islets was measured by glucose-stimulated insulin secretion (GSIS) and perifusion.

 Results

NAS mice showed higher glucose levels and lower insulin secretion in IPGTT than the control mice. There was no significant difference in insulin resistance. Total islet and β-cell masses were decreased in NAS mice. The number of large islets (≥250 µm) decreased while that of small islets (<250 µm) increased. Reduced insulin secretion was observed in GSIS and perifusion. Neurogenin3, neurogenic differentiation, and MAF bZIP transcription factor A levels increased in NAS mice.

 Conclusion

Our study provides that Notch1 inhibition decreased insulin secretion and decreased islet and β-cell masses. It is thought that Notch1 inhibition suppresses islet proliferation and induces differentiation of small islets. In conclusion, Notch signaling pathway may play an important role in β-cell mass determination and diabetes.

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Clinical Diabetes & Therapeutics
Early Assessment of the Risk for Gestational Diabetes Mellitus: Can Fasting Parameters of Glucose Metabolism Contribute to Risk Prediction?
Veronica Falcone, Grammata Kotzaeridi, Melanie Hanne Breil, Ingo Rosicky, Tina Stopp, Gülen Yerlikaya-Schatten, Michael Feichtinger, Wolfgang Eppel, Peter Husslein, Andrea Tura, Christian S. Göbl
Diabetes Metab J. 2019;43(6):785-793.   Published online March 12, 2019
DOI: https://doi.org/10.4093/dmj.2018.0218
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AbstractAbstract PDFPubReader   ePub   
Background

An early identification of the risk groups might be beneficial in reducing morbidities in patients with gestational diabetes mellitus (GDM). Therefore, this study aimed to assess the biochemical predictors of glycemic conditions, in addition to fasting indices of glucose disposal, to predict the development of GDM in later stage and the need of glucose-lowering medication.

Methods

A total of 574 pregnant females (103 with GDM and 471 with normal glucose tolerance [NGT]) were included. A metabolic characterization was performed before 15+6 weeks of gestation by assessing fasting plasma glucose (FPG), fasting insulin (FI), fasting C-peptide (FCP), and glycosylated hemoglobin (HbA1c). Thereafter, the patients were followed-up until the delivery.

Results

Females with NGT had lower levels of FPG, FI, FCP, or HbA1c at the early stage of pregnancy, and therefore, showed an improved insulin action as compared to that in females who developed GDM. Higher fasting levels of FPG and FCP were associated with a higher risk of developing GDM. Moreover, the predictive accuracy of this metabolic profiling was also good to distinguish the patients who required glucose-lowering medications. Indices of glucose disposal based on C-peptide improved the predictive accuracy compared to that based on insulin. A modified quantitative insulin sensitivity check index (QUICKIc) showed the best differentiation in terms of predicting GDM (area under the receiver operating characteristics curve [ROC-AUC], 72.1%) or need for pharmacotherapy (ROC-AUC, 83.7%).

Conclusion

Fasting measurements of glucose and C-peptide as well as the surrogate indices of glycemic condition could be used for stratifying pregnant females with higher risk of GDM at the beginning of pregnancy.

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Epidemiology
Clinical Characteristics of People with Newly Diagnosed Type 2 Diabetes between 2015 and 2016: Difference by Age and Body Mass Index
Kyoung Hwa Ha, Cheol Young Park, In Kyung Jeong, Hyun Jin Kim, Sang-Yong Kim, Won Jun Kim, Ji Sung Yoon, In Joo Kim, Dae Jung Kim, Sungrae Kim
Diabetes Metab J. 2018;42(2):137-146.   Published online February 14, 2018
DOI: https://doi.org/10.4093/dmj.2018.42.2.137
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AbstractAbstract PDFPubReader   ePub   
Background

We evaluated the clinical characteristics of insulin resistance and β-cell dysfunction in newly diagnosed, drug-naive people with type 2 diabetes by analyzing nationwide cross-sectional data.

Methods

We collected the clinical data of 912 participants with newly diagnosed diabetes from 83 primary care clinics and hospitals nationwide from 2015 to 2016. The presence of insulin resistance and β-cell dysfunction was defined as a homeostatic model assessment of insulin resistance (HOMA-IR) value ≥2.5 and fasting C-peptide levels <1.70 ng/mL, respectively.

Results

A total of 75.1% and 22.6% of participants had insulin resistance and β-cell dysfunction, respectively. The proportion of participants with insulin resistance but no β-cell dysfunction increased, and the proportion of participants with β-cell dysfunction but no insulin resistance decreased as body mass index (BMI) increased. People diagnosed with diabetes before 40 years of age had significantly higher HOMA-IR and BMI than those diagnosed over 65 years of age (HOMA-IR, 5.0 vs. 3.0; BMI, 28.7 kg/m2 vs. 25.1 kg/m2). However, the β-cell function indices were lower in people diagnosed before 40 years of age than in those diagnosed after 65 years of age (homeostatic model assessment of β-cell function, 39.3 vs. 64.9; insulinogenic index, 10.3 vs. 18.7; disposition index, 0.15 vs. 0.25).

Conclusion

We observed that the main pathogenic mechanism of type 2 diabetes is insulin resistance in participants with newly diagnosed type 2 diabetes. In addition, young adults with diabetes are more likely to have higher insulin resistance with obesity and have higher insulin secretory defect with severe hyperglycemia in the early period of diabetes than older populations.

Citations

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  • Response: Clinical Characteristics of People with Newly Diagnosed Type 2 Diabetes between 2015 and 2016: Difference by Age and Body Mass Index (Diabetes Metab J2018;42:137-46)
    Kyoung Hwa Ha, Dae Jung Kim, Sungrae Kim
    Diabetes & Metabolism Journal.2018; 42(3): 251.     CrossRef
  • Letter: Clinical Characteristics of People with Newly Diagnosed Type 2 Diabetes between 2015 and 2016: Difference by Age and Body Mass Index (Diabetes Metab J 2018;42:137-46)
    Ah Reum Khang
    Diabetes & Metabolism Journal.2018; 42(3): 249.     CrossRef
Others
Comparison of the Usefulness of the Updated Homeostasis Model Assessment (HOMA2) with the Original HOMA1 in the Prediction of Type 2 Diabetes Mellitus in Koreans
Young Seok Song, You-Cheol Hwang, Hong-Yup Ahn, Cheol-Young Park
Diabetes Metab J. 2016;40(4):318-325.   Published online May 27, 2016
DOI: https://doi.org/10.4093/dmj.2016.40.4.318
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AbstractAbstract PDFPubReader   ePub   
Background

The original homeostasis model assessment (HOMA1) and the updated HOMA model (HOMA2) have been used to evaluate insulin resistance (IR) and β-cell function, but little is known about the usefulness of HOMA2 for the prediction of diabetes in Koreans. The aim of this study was to demonstrate the usefulness of HOMA2 as a predictor of type 2 diabetes mellitus in Koreans without diabetes.

Methods

The study population consisted of 104,694 Koreans enrolled at a health checkup program and followed up from 2001 to 2012. Participants were divided into a normal glucose tolerance (NGT) group and a pre-diabetes group according to fasting glucose and glycosylated hemoglobin levels. Anthropometric and laboratory data were measured at the baseline checkup, and HOMA values were calculated at the baseline and follow-up checkups. The hazard ratios (HRs) of the HOMA1 and HOMA2 values and the prevalence of diabetes at follow-up were evaluated using a multivariable Cox proportional hazards model and Kaplan-Meier analysis.

Results

After adjusting for several diabetes risk factors, all of the HOMA values except 1/HOMA1-β and 1/HOMA2-β in the NGT group were significant predictors of the progression to diabetes. In the NGT group, there was no significant difference in HOMA1-IR (HR, 1.09; 95% confidence interval [CI], 1.04 to 1.14) and HOMA2-IR (HR, 1.11; 95% CI, 1.04 to 1.19). However, in the pre-diabetes group, 1/HOMA2-β was a more powerful marker (HR, 1.29; 95% CI, 1.26 to 1.31) than HOMA1-IR (HR, 1.23; 95% CI, 1.19 to 1.28) or 1/HOMA1-β (HR, 1.14; 95% CI, 1.12 to 1.16). In the non-diabetic group (NGT+pre-diabetes), 1/HOMA2-β was also a stronger predictor of diabetes (HR, 1.27; 95% CI, 1.25 to 1.29) than HOMA1-IR (HR, 1.14; 95% CI, 1.12 to 1.15) or 1/HOMA1-β (HR, 1.13; 95% CI, 1.11 to 1.14).

Conclusion

HOMA2 is more predictive than HOMA1 for the progression to diabetes in pre-diabetes or non-diabetic Koreans.

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The Insulin Resistance but Not the Insulin Secretion Parameters Have Changed in the Korean Population during the Last Decade
Hae Kyung Yang, Jin Hee Lee, In-Young Choi, Hyuk Sang Kwon, Jeong Ah Shin, Seung Hee Jeong, Seung-Hwan Lee, Jae Hyoung Cho, Ho Young Son, Kun Ho Yoon
Diabetes Metab J. 2015;39(2):117-125.   Published online April 20, 2015
DOI: https://doi.org/10.4093/dmj.2015.39.2.117
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AbstractAbstract PDFPubReader   ePub   
Background

This study aimed to compare the patterns of insulin secretion and resistance between Korean subjects in the 1990s and 2000s.

Methods

Insulin secretion and resistance indices were calculated from subjects who underwent 75-g oral glucose tolerance tests in the year 1997 to 1999 and 2007 to 2011 at the Seoul St. Mary's Hospital, Korea.

Results

A total of 578 subjects from the 1990s (mean age, 48.5 years) and 504 subjects from the 2000s (mean age, 50.2 years) were enrolled. Compared with the subjects from the 1990s, those from the 2000s exhibited increased insulin resistance (increased homeostatic model assessment for insulin resistance), and reduced insulin sensitivity (reduced Matsuda index and quantitative insulin sensitivity check index), regardless of their glucose tolerance status. However, insulinogenic index did not reveal significant differences between the 2 decades in subjects with or without diabetes. A distinct relationship was confirmed between Matsuda index and total area under the curve (insulin/glucose) in each glucose tolerance group. The mean product of the Matsuda index and the total area under the curve (insulin/glucose) as well as the oral disposition index, was lower in subjects with normal glucose tolerance from the 2000s than in those from the 1990s.

Conclusion

After rapid economic growth and changes in lifestyle patterns, insulin resistance has worsened across the glucose tolerance status; however, the insulin secretory function remained unchanged, which resulted in an increase in the susceptibility to the development of type 2 diabetes mellitus among Korean subjects without diabetes. We could not rule out the potential selection bias and therefore, further studies in general Korean population are needed.

Citations

Citations to this article as recorded by  
  • Evolving Characteristics of Type 2 Diabetes Mellitus in East Asia
    Joonyub Lee, Kun-Ho Yoon
    Endocrinology and Metabolism.2025; 40(1): 57.     CrossRef
  • Insulin Resistance, Non-Alcoholic Fatty Liver Disease and Type 2 Diabetes Mellitus: Clinical and Experimental Perspective
    Inha Jung, Dae-Jeong Koo, Won-Young Lee
    Diabetes & Metabolism Journal.2024; 48(3): 327.     CrossRef
  • A Randomized Crossover Study Comparing the Effects of Diabetes-Specific Formula with Common Asian Breakfasts on Glycemic Control and Satiety in Adults with Type 2 Diabetes Mellitus
    Sing Teang Kong, Dieu Thi Thu Huynh, Weerachai Srivanichakorn, Weerapan Khovidhunkit, Chaiwat Washirasaksiri, Tullaya Sitasuwan, Chengrong Huang, Swapnil Paunikar, Menaka Yalawar, Siew Ling Tey
    Diabetology.2024; 5(4): 447.     CrossRef
  • Longitudinal Changes in Insulin Resistance, Beta-Cell Function and Glucose Regulation Status in Prediabetes
    Chul-Hee Kim, Hong-Kyu Kim, Eun-Hee Kim, Sung-Jin Bae, Jaewon Choe, Joong-Yeol Park
    The American Journal of the Medical Sciences.2018; 355(1): 54.     CrossRef
  • Association of serum 25-hydroxyvitamin D and diabetes-related factors in Korean adults without diabetes: The Fifth Korea National Health and Nutrition Examination Survey 2010–2012
    Hyunah Kim, Hyunyong Lee, Hyeon Woo Yim, Hun-Sung Kim
    Primary Care Diabetes.2018; 12(1): 59.     CrossRef
  • Long‐term effects on glycaemic control and β‐cell preservation of early intensive treatment in patients with newly diagnosed type 2 diabetes: A multicentre randomized trial
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    Diabetes, Obesity and Metabolism.2018; 20(5): 1121.     CrossRef
  • Four Plasma Glucose and Insulin Responses to a 75 g OGTT in Healthy Young Japanese Women
    Kei Takahashi, Hidetaka Nakamura, Hiroshi Sato, Hideto Matsuda, Kazuo Takada, Tomiko Tsuji
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Hexane Extract of Orthosiphon stamineus Induces Insulin Expression and Prevents Glucotoxicity in INS-1 Cells
Hae-Jung Lee, Yoon-Jung Choi, So-Young Park, Jong-Yeon Kim, Kyu-Chang Won, Jong-Keun Son, Yong-Woon Kim
Diabetes Metab J. 2015;39(1):51-58.   Published online February 16, 2015
DOI: https://doi.org/10.4093/dmj.2015.39.1.51
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AbstractAbstract PDFPubReader   ePub   
Background

Hyperglycemia, a characteristic feature of diabetes, induces glucotoxicity in pancreatic β-cells, resulting in further impairment of insulin secretion and worsening glycemic control. Thus, preservation of insulin secretory capacity is essential for the management of type 2 diabetes. In this study, we evaluated the ability of an Orthosiphon stamineus (OS) extract to prevent glucotoxicity in insulin-producing cells.

Methods

We measured insulin mRNA expression and glucose-stimulated insulin secretion (GSIS) in OS-treated INS-1 cells after exposure to a high glucose (HG; 30 mM) concentration.

Results

The hexane extract of OS elevated mRNA expression of insulin as well as pancreatic and duodenal homeobox-1 of INS-1 cells in a dose-dependent manner. The hexane OS extract also increased the levels of phosphorylated phosphatidylinositol 3-kinase (PI3K) in a concentration-dependent manner. Additionally, Akt phosphorylation was elevated by treatment with 100 and 200 µmol of the hexane OS extract. Three days of HG exposure suppressed insulin mRNA expression and GSIS; these expressions were restored by treatment with the hexane OS extract. HG elevated peroxide levels in the INS-1 cells. These levels were unaffected by OS treatment under both normal and hyperglycemic conditions.

Conclusion

Our results suggested that the hexane extract of OS elevates insulin mRNA expression and prevents glucotoxicity induced by a 3-day treatment with HG. This was associated with the activation of PI-3K and Akt.

Citations

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  • Effect of Triclisia subcordata Oliv. (Menispermaceae) leaf on alloxan-induced diabetic rats
    Mubo Adeola Sonibare, Samuel Abayomi Adebodun, Akingbolabo Daniel Ogunlakin
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    Yun Luo, Yue Liu, Quan Wen, Yulin Feng, Ting Tan
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    Krista Minéia Wartchow, Letícia Rodrigues, Lucas Zingano Suardi, Barbara Carolina Federhen, Nicholas Guerini Selistre, Carlos-Alberto Gonçalves, Patrícia Sesterheim
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    Dhamraa Waleed Al-dualimi, Aman Shah Abdul Majid, Sarah Furqan Faisal Al-Shimary, Amal Aziz Al-Saadi, Raghdaa Al Zarzour, Muhammad Asif, Chern Ein Oon, Amin Malik Shah Abdul Majid
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Impact of Serum Triglyceride and High Density Lipoprotein Cholesterol Levels on Early-Phase Insulin Secretion in Normoglycemic and Prediabetic Subjects
Masanori Shimodaira, Tomohiro Niwa, Koji Nakajima, Mutsuhiro Kobayashi, Norinao Hanyu, Tomohiro Nakayama
Diabetes Metab J. 2014;38(4):294-301.   Published online August 20, 2014
DOI: https://doi.org/10.4093/dmj.2014.38.4.294
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AbstractAbstract PDFPubReader   ePub   
Background

Increased triglycerides (TGs) and decreased high density lipoprotein cholesterol (HDL-C) levels are established as diabetic risks for nondiabetic subjects. The aim of this study was to investigate the relationship among TG, HDL-C, TG/HDL-C ratio, and early-phase insulin secretion in normoglycemic and prediabetic subjects.

Methods

We evaluated 663 Japanese subjects who underwent the 75-g oral glucose tolerance test. On the basis of these results, the subjects were divided into four groups: those with normal glucose tolerance (NGT; n=341), isolated impaired fasting glucose (i-IFG; n=211), isolated impaired glucose tolerance (i-IGT; n=71), and combined IFG and IGT (IFG+IGT; n=40). Insulin secretion was estimated by the insulinogenic index (IGI) (Δinsulin/Δglucose [30 to 0 minutes]) and disposition index (DI) (IGI/homeostasis model assessment of insulin resistance).

Results

In prediabetic subjects (i-IFG, i-IGT, and IFG+IGT), linear regression analyses revealed that IGI and DI were positively correlated with HDL-C levels. Moreover, in subjects with i-IGT and (IFG+IGT), but not with i-IFG, the indices of insulin secretion were negatively correlated with the log-transformed TG and TG/HDL-C ratio. In both the subjects with i-IGT, multivariate linear regression analyses revealed that DI was positively correlated with HDL-C and negatively with log-transformed TG and TG/HDL-C ratio. On the other hand, in subjects with NGT, there was no association between insulin secretion and lipid profiles.

Conclusion

These results revealed that serum TG and HDL-C levels have different impacts on early-phase insulin secretion on the basis of their glucose tolerance status.

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Reviews
Neonatal Diabetes Caused by Activating Mutations in the Sulphonylurea Receptor
Peter Proks
Diabetes Metab J. 2013;37(3):157-164.   Published online June 14, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.3.157
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  • 64 Download
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AbstractAbstract PDFPubReader   ePub   

Adenosine triphosphate (ATP)-sensitive potassium (KATP) channels in pancreatic β-cells play a crucial role in insulin secretion and glucose homeostasis. These channels are composed of two subunits: a pore-forming subunit (Kir6.2) and a regulatory subunit (sulphonylurea receptor-1). Recent studies identified large number of gain of function mutations in the regulatory subunit of the channel which cause neonatal diabetes. Majority of mutations cause neonatal diabetes alone, however some lead to a severe form of neonatal diabetes with associated neurological complications. This review focuses on the functional effects of these mutations as well as the implications for treatment.

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A Systematic Review of Oxidative Stress and Safety of Antioxidants in Diabetes: Focus on Islets and Their Defense
Udayakumar Karunakaran, Keun-Gyu Park
Diabetes Metab J. 2013;37(2):106-112.   Published online April 16, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.2.106
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AbstractAbstract PDFPubReader   ePub   

A growing body of evidence suggests that hyperglycemia-induced oxidative stress plays an important role in diabetic complications, especially β-cell dysfunction and failure. Under physiological conditions, reactive oxygen species serve as second messengers that facilitate signal transduction and gene expression in pancreatic β-cells. However, under pathological conditions, an imbalance in redox homeostasis leads to aberrant tissue damage and β-cell death due to a lack of antioxidant defense systems. Taking into account the vulnerability of islets to oxidative damage, induction of endogenous antioxidant enzymes or exogenous antioxidant administration has been proposed as a way to protect β-cells against diabetic insults. Here, we consider recent insights into how the redox response becomes deregulated under diabetic conditions, as well as the therapeutic benefits of antioxidants, which may provide clues for developing strategies aimed at the treatment or prevention of diabetes associated with β-cell failure.

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Fuel-Stimulated Insulin Secretion Depends upon Mitochondria Activation and the Integration of Mitochondrial and Cytosolic Substrate Cycles
Gary W. Cline
Diabetes Metab J. 2011;35(5):458-465.   Published online October 31, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.5.458
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AbstractAbstract PDFPubReader   ePub   

The pancreatic islet β-cell is uniquely specialized to couple its metabolism and rates of insulin secretion with the levels of circulating nutrient fuels, with the mitochondrial playing a central regulatory role in this process. In the β-cell, mitochondrial activation generates an integrated signal reflecting rates of oxidativephosphorylation, Kreb's cycle flux, and anaplerosis that ultimately determines the rate of insulin exocytosis. Mitochondrial activation can be regulated by proton leak and mediated by UCP2, and by alkalinization to utilize the pH gradient to drive substrate and ion transport. Converging lines of evidence support the hypothesis that substrate cycles driven by rates of Kreb's cycle flux and by anaplerosis play an integral role in coupling responsive changes in mitochondrial metabolism with insulin secretion. The components and mechanisms that account for the integrated signal of ATP production, substrate cycling, the regulation of cellular redox state, and the production of other secondary signaling intermediates are operative in both rodent and human islet β-cells.

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The Causes and Consequences of Low Levels of High Density Lipoproteins in Patients with Diabetes
Philip J. Barter
Diabetes Metab J. 2011;35(2):101-106.   Published online April 30, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.2.101
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AbstractAbstract PDFPubReader   ePub   

Type 2 diabetes is commonly accompanied by a low level of high density lipoprotein cholesterol (HDL-C) that contributes to the increased cardiovascular risk associated with this condition. Given that HDLs have the ability to improve increase the uptake of glucose by skeletal muscle and to stimulate the secretion of insulin from pancreatic beta cells the possibility arises that a low HDL concentration in type 2 diabetes may also contribute to a worsening of diabetic control. Thus, there is a double case for raising the level of HDL-C in patients with type 2 diabetes: to reduce cardiovascular risk and to improve glycemic control. Approaches to raising HDL-C include lifestyle factors such as weight reduction, increased physical activity and stopping smoking. Of currently available drugs, the most effective is niacin. Newer formulations of niacin are reasonably well tolerated and have the ability to increase HDL-C by up to 30%. The effect of niacin on cardiovascular events in type 2 diabetes is currently being tested in a large-scale clinical outcome trial.

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Original Articles
Insulin Secretion and Incretin Hormone Concentration in Women with Previous Gestational Diabetes Mellitus
Sung Hoon Yu, Bongjun Cho, Yejin Lee, Eunhye Kim, Sung Hee Choi, Soo Lim, Ka Hee Yi, Young Joo Park, Kyong Soo Park, Hak Chul Jang
Diabetes Metab J. 2011;35(1):58-64.   Published online February 28, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.1.58
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AbstractAbstract PDFPubReader   ePub   
Background

We examined the change in the levels of incretin hormone and effects of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) on insulin secretion in women with previous gestational diabetes (pGDM).

Methods

A 75-g oral glucose tolerance test (OGTT) was conducted on 34 women with pGDM. In addition, 11 women with normal glucose tolerance, matched for age, height and weight, were also tested. The insulin, GIP, GLP-1, and glucagon concentrations were measured, and their anthropometric and biochemical markers were also measured.

Results

Among 34 women with pGDM, 18 had normal glucose tolerance, 13 had impaired glucose tolerance (IGT) and 1 had diabetes. No significant differences were found in GLP-1 concentration between the pGDM and control group. However, a significantly high level of glucagon was present in the pGDM group at 30 minutes into the OGTT. The GIP concentration was elevated at 30 minutes and 60 minutes in the pGDM group. With the exception of the 30-minute timepoint, women with IGT had significantly high blood glucose from 0 to 120 minutes. However, there was no significant difference in insulin or GLP-1 concentration. The GIP level was significantly high from 0 to 90 minutes in patients diagnosed with IGT.

Conclusion

GLP-1 secretion does not differ between pGDM patients and normal women. GIP was elevated, but that does not seem to induce in increase in insulin secretion. Therefore, we conclude that other factors such as heredity and environment play important roles in the development of type 2 diabetes.

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gamma-glutamylcysteine Synthetase (gamma-GCS) mRNA Expression in INS-1 Cells and Patients with Type 2 Diabetes Mellitus.
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AbstractAbstract PDF
BACKGROUND
Hyperglycemia is a well-recognized pathogenic factor of long term complications in diabetes mellitus and hyperglycemia also generates reactive oxygen species (ROS) in beta cells when ROS accumulate in excess for prolonged periods of time, they cause chronic oxidative stress and adverse effects. Unfortunately, the islet contacts low capacity of endogenous antioxidant effects. But, gamma-glutamylcysteine synthetase (gamma-GCS), the rate-limiting enzyme for glutathione synthesis, is well represented in islets. METHODS: This study is to evaluate the changes in the activity of gamma-GCS, glutathione in beta-cells exposed to high glucose, in pancreatic tissue of OLETF (Otsuka Long Evans Tokushima Fatty) and LETO (Long-Evans Tokushima Otsuka) rats, in leukocytes from patients with Korean type 2 DM (T2DM) and to disclose the effects of high blood glucose on this impairment in patients with T2DM. We divided our patients into 3 groups by HbA1c (controls: n = 20, well controls diabetes: n=24, poorly controlled diabetes: n = 36). RESULTS: We observed that decreased glutathione level, gamma-GCS expression, glucose-stimulated (GSIS) and increased intracellular peroxide level in the INS-1 cells exposed to 30 mM glucose condition. Also decreased glutathione level at erythrocytes, gamma-GCS expression at leukocytes and increased oxidized LDL, MDA (malondialdehyde) level at plasma from patients with T2DM compared to controls (esp, poorly controlled patients). CONCLUSION: These results suggest that insufficient antioxidant defenses by the glutathione pathway may be one of the factors responsible for development of complications in T2DM.
Clinical Characteristics of Korean Type 2 Diabetic Patients According to Insulin Secretion and Insulin Resistance.
Kyoung Eun Song, Dae Jung Kim, Ji Won Park, Hong Keun Cho, Kwan Woo Lee, Kap Bum Huh
Korean Diabetes J. 2007;31(2):123-129.   Published online March 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.2.123
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AbstractAbstract PDF
BACKGROUND
Korean type 2 diabetic patients are known to differ from western diabetes because of their unique characteristics, such as non-obese but centrally obese anthropometry and relatively more insulin secretory defects than insulin resistance compared to western diabetic patients. METHODS: We recruited 1,646 diabetic patients in the present study and excluded the 45 patients with fasting C-peptide < 0.20 nmol/L. We had assessed insulin secretion by fasting serum C-peptide level and insulin resistance by short insulin tolerance test (Kitt ; rate constant for plasma glucose disappearance, %/min) in the private diabetes clinic. The insulin secretory defect was divided by severe (C-peptide < 0.37 nmol/L), moderate (C-peptide 0.37~0.56 nmol/L), and normal (C-peptide > or = 0.57 nmol/L) group. The insulin resistance was divided by insulin resistant (IR) (Kitt < 2.5 %/min) and insulin sensitive (IS) (Kitt > or = 2.5 %/min) group. RESULTS: We analysed the data of 1,601 type 2 diabetic patients (831 men and 770 women, age 56.5 +/- 10.8 years, duration of diabetes 9.6 +/- 7.3 years). The prevalence of BMI > or = 25.0 kg/m2 is 42.5% and BMI > or = 23.0 kg/m2 is 70.2%. The prevalence of abdominal obesity (waist > or = 90 cm in men and 80 cm in women) is 45.2% (36.0% and 55.2%, respectively in men and women). Fasting C-peptide level is 0.64 +/- 0.29 nmol/L and Kitt value is 2.03 +/- 0.96%/min. According to fasting C-peptide level, the degree of insulin secretory defect were severe (13.1%), moderate (33.0%) and normal (53.9%). According to Kitt value, the IR group is 70.6% and the IS group is 29.4%. CONCLUSION: Obese type 2 diabetes is markedly increasing in Korea. Therefore, the major problem in Korean type 2 diabetic patients is being changed into insulin resistance instead of insulin secretory defect.

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    Ye Rin Kim, Eun-young Kim, Seong Uk Lee, Young Wan Kim, Yoon Hee Kim
    Journal of the Korean Society of Food Science and Nutrition.2022; 51(9): 894.     CrossRef
  • Effect of Nutrition Counseling by Nutrition Care Process on Diet Therapy Practice and Glycemic Control in Type 2 Diabetic Patients
    Tae-Jeong Bae, Na-Eun Jeon, Soo-Kyong Choi, Jung-Sook Seo
    Korean Journal of Community Nutrition.2020; 25(3): 214.     CrossRef
  • Calpain-10 and Adiponectin Gene Polymorphisms in Korean Type 2 Diabetes Patients
    Ji Sun Nam, Jung Woo Han, Sang Bae Lee, Ji Hong You, Min Jin Kim, Shinae Kang, Jong Suk Park, Chul Woo Ahn
    Endocrinology and Metabolism.2018; 33(3): 364.     CrossRef
  • Obesity and Insulin Resistance According to Age in Newly Diagnosed Type 2 Diabetes Patients in Korea
    Ju Won Lee, Nam Kyu Kim, Hyun Joon Park, Jun Yeob Lee, Seon Yoon Choi, Eun Mi Lee, So Young Ock, Su Kyoung Kwon, Young Sik Choi, Bu Kyung Kim
    Kosin Medical Journal.2016; 31(2): 157.     CrossRef
  • The Insulin Resistance but Not the Insulin Secretion Parameters Have Changed in the Korean Population during the Last Decade
    Hae Kyung Yang, Jin Hee Lee, In-Young Choi, Hyuk Sang Kwon, Jeong Ah Shin, Seung Hee Jeong, Seung-Hwan Lee, Jae Hyoung Cho, Ho Young Son, Kun Ho Yoon
    Diabetes & Metabolism Journal.2015; 39(2): 117.     CrossRef
  • The Effects of Low-Calorie Diets on Abdominal Visceral Fat, Muscle Mass, and Dietary Quality in Obese Type 2 Diabetic Subjects (Korean Diabetes J 2009;33:526-36)
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    Korean Diabetes Journal.2010; 34(1): 68.     CrossRef
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  • The Effects of Low-Calorie Diets on Abdominal Visceral Fat, Muscle Mass, and Dietary Quality in Obese Type 2 Diabetic Subjects (Korean Diabetes J 2009;33:526-36)
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    Korean Diabetes Journal.2010; 34(1): 66.     CrossRef
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Role of Glucocorticoid Receptor on Insulin Secretion and Synthesis in INS-1 Cells.
Ju Yeon Yang, Myong Su Kang, Tak Ho Song, In Kook Jeong, Pyong Ju Seo, Hee Jin Kim
Korean Diabetes J. 2006;30(6):428-434.   Published online November 1, 2006
DOI: https://doi.org/10.4093/jkda.2006.30.6.428
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BACKGROUND
Glucocorticoids play important roles in the regulation of glucose homeostasis. It is well known that glucocorticoids reduce hepatic and peripheral tissue sensitivity to insulin, but the roles of glucocorticoids on insulin secretion and synthesis in pancreatic beta cells are still unclear. We have investigated the direct effects of glucocorticoids on insulin secretion and synthesis in rat insulinoma (INS-1) cells. METHODS: Insulin content and 11.2 mM glucose-stimulated insulin secretion (GSIS) were measured in INS-1 cells after culture with or without 1 micrometer dexamethasone (DEX). Preproinsulin mRNA levels were analyzed by real-time RT-PCR and normalized to the internal control. Effect of RU486 on DEX-induced inhibition of GSIS and preproinsulin mRNA synthesis was evaluated. RESULTS: Insulin content of INS-1 cells cultured in RPMI containing 11.2 mM glucose in the presence of DEX was not different from that of control cells. After 1-h preincubation in 2.8 mM glucose, basal insulin secretion from cells treated with DEX did not differ from that of controls, but GSIS was significantly reduced in the cells treated with DEX in comparison to control cells. The expression of preproinsulin mRNA relative to beta-actin mRNA was also lower in the cells treated with DEX. Glucocorticoid receptor antagonist improved DEX-induced inhibition of GSIS and preproinsulin mRNA synthesis. CONCLUSION: DEX inhibited GSIS and preproinsulin mRNA synthesis in INS-1 cells. Glucocorticoid receptor antagonist ameliorated the reduced GSIS and preproinsulin mRNA synthesis induced by DEX.
Insulin Secretion and Insulin Resistance in Newly Diagnosed, Drug Naive Prediabetes and Type 2 Diabetes Patients With/Without Metabolic Syndrome.
Sang Youl Rhee, Suk Chon, Seungjoon Oh, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Jeong Taek Woo
Korean Diabetes J. 2006;30(3):198-206.   Published online May 1, 2006
DOI: https://doi.org/10.4093/jkda.2006.30.3.198
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AbstractAbstract PDF
BACKGROUND
To evaluate the relationships between deterioration in insulin secretion and aggravated insulin resistance in patients with newly diagnosed prediabetes (preDM) and type 2 diabetes mellitus (T2DM) according to the presence of metabolic syndrome (MS). METHODS: We performed oral glucose tolerance test (OGTT) on 322 drug naive subjects with a history of hyperglycemia of < or = 3 months, and divided these patients into 3 groups, normal glucose tolerance (NGT), preDM (IFG and/or IGT) and T2DM. We also diagnosed these subjects with respect to MS according to ATP III criteria modified by Asia-Pacific guidelines and compared IGI and HOMA-IR in the 3 groups. RESULTS: According to OGTT, 63 subjects were diagnosed with NGT, 81 with preDM, and 178 with T2DM. Using modified ATP III criteria, 218 (67.7%) subjects were diagnosed as MS. When compare groups stratified by the presence of MS, preDM and T2DM groups with MS showed significantly higher mean HOMA-IR and IGI than those without MS. When compare groups with respect to glucose tolerance, NGT, preDM, and T2DM subgroups in MS group showed significant higher HOMA-IR and lower IGI according to glucose tolerance. However, NGT, preDM, and T2DM subgroups in non-MS group showed a significant decrease in IGI but no significant difference in HOMA-IR as glucose tolerance worsened. CONCLUSION: Deterioration in IGI and aggravation of HOMA-IR are both important in the primary pathogenesis of diabetes in those with MS. However, IGI deterioration may be the only important factor in the primary pathogenesis of T2DM in the absence of MS.

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  • The Relationship between β-cell Function and Nutrient Intakes in Korean Adult - Using 4thKorea National Health and Nutrition Examination Survey 2009 -
    You Mi Lee, Hye Kyung Chung, Heejin Kimm, Sun Ha Jee
    Korean Journal of Community Nutrition.2012; 17(2): 243.     CrossRef
The Association of Family History of Diabetes and Obesity in the Development of Type 2 Diabetes.
Wan Sub Shim, Hae Jin Kim, Soo Kyung Kim, Seung Jin Han, Eun Seok Kang, Yu Mie Rhee, Chul Woo Ahn, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Bong Soo Cha
Korean Diabetes J. 2005;29(6):540-547.   Published online November 1, 2005
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AbstractAbstract PDF
BACKGROUND
Type 2 diabetes is characterized by defects in both insulin secretion and insulin action. Type 2 diabetes has a strong genetic basis, and obesity is also known as a important risk factor for development of diabetes. The relative effects of obesity and family history of diabetes (FHx) to develop diabetes have not been well characterized. The aim of this study was to analyze the relative role of insulin resistance and insulin secretion in the newly diagnosed type 2 diabetic patients according to the presence of FHx and obesity. METHOD: We evaluated the presence of FHx, fasting and postprandial glucose, C-peptide and insulin in 219 newly diagnosed type 2 diabetic patients without the history of drug therapy from Jan. 2003 to Oct. 2004. RESULT: The mean age of patients was 54.7+/-10.2(yr) and the mean BMI was 25.5+/-3.0 kg/m2. The patients with FHx develop diabetes earlier than them without FHx. BMI, fasting glucose, postprandial glucose, fasting C-peptide and HOMAIR value were not different between groups. But postprandial C-peptide, fasting insulin, postprandial insulin and HOMAbeta-cell value were significantly lower in patient with FHx than in them without FHx. Interestingly, obese (BMI > or = 25kg/m2) patients with FHx developed diabetes earlier than nonobese (BMI <25kg/m2) patients with FHx. CONCLUSION: Obesity plays an important role in the determination of the earlier onset of diabetes in patients with FHx. Intentional prevention of obesity may be an important means to prevent, at least delay, the onset of diabetes in the subjects with FHx.
Clinical Meaning of Postprandial Insulin Secretory Function in Korean Type 2 Diabetes Mellitus.
Wan Sub Shim, Soo Kyung Kim, Hae Jin Kim, Se Eun Park, Eun Seok Kang, Yu Mie Rhee, Chul Woo Ahn, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Bong Soo Cha
Korean Diabetes J. 2005;29(4):367-377.   Published online July 1, 2005
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BACKGROUND
Impaired pancreatic beta-cell responsiveness is associated with type 2 diabetes mellitus. Postprandial insulin deficiency is closely related with fasting plasma glucose, HbA1c and insulin responses to meals, but most studies examining postprandial beta-cell responsiveness have been limited by the small number of type 2 diabetic patients examined. The aim of this study was to evaluate fasting and postprandial insulin secretions in relation to the duration of diabetes, BMI and glycemic control in a large number of patients with variable disease durations. METHODS: We evaluated the fasting plasma glucose, insulin, C-peptide, HbA1c, BMI, postprandial 2 hour glucose, insulin and C-peptide in 1,170(male 662, female 508, age 54.6+/-1.6 years, duration of diabetes 5.2+/-6.3 years, BMI 25.4+/-3.3kg/m(2)) type 2 diabetic patients. The delta C-peptide, delta insulin, fasting(M0) and postprandial(M1) pancreatic beta-cell responsiveness were also calculated. The subjects were divided into three groups according to their duration of diabetes, BMI, and fasting and postprandial C-peptide levels. After adjusting for age, sex and BMI, the correlation of diabetes and HbA1c were correlated parameters. RESULTS: In the group of patients whose duration of diabetes was longer than 10 years, the BMI, fasting, postprandial and delta C-peptide, and M0 and M1 were significantly lower, but age, fasting and postprandial glucose, as well as HbA1c were significantly higher than those in the other groups. There were no significant differences in the fasting and postprandial glucose and HbA1c according to their fasting C-peptide tertiles. However, in the group of patients with the highest postprandial C-peptide tertile, the fasting and postprandial glucose and HbA1c were significantly lower than those in the other groups. The duration of diabetes, after adjustment of age, sex and BMI, was negatively correlated with the fasting, postprandial and delta C-peptide, M0 and M1, but was positively correlated with the fasting and postprandial 2 hour glucose and HbA1c. The HbA1c after adjustment of age, sex and BMI, was positively correlated with duration of diabetes, and fasting and postprandial glucose, but was negatively correlated with fasting postprandial and delta C-peptide, M0 and M1. CONCLUSION: Although the fasting and postprandial insulin secretions were decreased with duration of diabetes, the decrease in the postprandial insulin secretion was more prominent. The postprandial pancreatic responsiveness may be a more important factor in predicting glycemic control in Korean type 2 diabetic patients than the fasting pancreatic responsiveness.
Analysis of the Relative Importance of Insulin Resistance and Insulin Secretion Defect by Homeostasis Model Assessment in Korean Type 2 Diabetic Patients.
Wan Sub Shim, Soo Kyung Kim, Hae Jin Kim, Jae Hoon Moon, Eun Seok Kang, Yu Mie Rhee, Chul Woo Ahn, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Bong Soo Cha
Korean Diabetes J. 2005;29(3):206-214.   Published online May 1, 2005
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AbstractAbstract PDF
BACKGROUND
Type 2 diabetes is characterized by defects in both insulin secretion and insulin sensitivity. However, the relative importance of insulin secretion and insulin resistance in Korean type 2 diabetic patients has not been well characterized in any study that has included a large number of subjects. Therefore, this study aimed to evaluate the relative importance of insulin sensitivity and the function of the beta cell in Korean type 2 diabetic patients. METHODS: We applied the HOMA model to 1,162 type 2 diabetic patients (654 males and, 508 females) who did not use insulin and we assessed HOMAIR and HOMAbetacell & its relation to the other parameters. RESULTS: The HOMAIR of Korean type 2 diabetic patients was 2.29(range: 0.31~37.17) and the HOMAbetacell of Korean type 2 diabetic patients was 32.17(range: 1.04~1310.79). The HOMAIR of Korean type 2 diabetic male patients was 2.15(range: 0.31~16.6) and that of Korean type 2 diabetic female patients was 2.47(range: 0.36~37.17). The HOMAbetacell of Korean type 2 diabetic male patients was 30.1(range: 1.04~462.34) and that of Korean type 2 diabetic female patients was 35.42(range: 2.60~1310.79). The HOMAIR and HOMAbetacell were significantly higher in females than males. There was no significant correlation between HOMAIR and age, and the duration of diabetes, but there was significant correlation between HOMAIR and BMI, fasting glucose, HbA1c and the fasting insulin. There was no significant correlation between age and HOMAbetacell. However, there was significant correlation between HOMAbetacell and BMI, the duration of diabetes, the fasting glucose, HbA1c and the fasting insulin. The longer the duration of diabetes, the more the HOMAbetacell was decreased but there was no change of HOMAIR with respect to the duration of diabetes. As expected, the subjects with a lower HOMAIR and a higher HOMAbetacell had the best glycemic control. Those with a higher HOMAIR and lower HOMAbetacell had the worst glycemic control although they had taken larger amount of oral hypoglycemic agents. Interestingly, the patients with a lower HOMAIR and higher HOMAbetacell had better glycemic control than those patients with a higher HOMAIR and lower HOMAbetacell. CONCLUSION: Both insulin secretion and insulin resistance are important in glycemic control but it seems that insulin secretion is a more important factor in glycemic control than insulin resistance in the Korean type 2 diabetic patients
Effects of Aging and Obesity on Insulin Secretion and Sensitivity.
J Y Kim, J H Jee, H J Kim, B W Lee, Y J Chung, J H Chung, Y K Min, M S Lee, M K Lee, K W Kim
Korean Diabetes J. 2005;29(1):39-47.   Published online January 1, 2005
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AbstractAbstract PDF
BACKGROUND
Type 2 diabetes is occurring in epidemic proportions worldwide and aging has been defined as one of the risk factors for the progression to diabetes. The mechanism responsible for deterioration of glucose tolerance with aging is still unclear. It has been debated whether this deterioration results from an abnormal beta cell secretory function or/and decreased insulin sensitivity, from the aging process per se, or some other factors, such as an increase in BMI and abdominal fat. The changes in the insulin secretion and sensitivity were assessed in relation to aging and obesity, and the association between obesity and factors influencing glucose homeostasis in obese subjects evaluated. METHODS: 530 individuals, aged 24 to 75 years, having undergone a 75 g OGTT were enrolled, and the insulinogenic index and HOMA-IR calculated for each subject. 212 individuals were obese, i.e. a BMI above 25, which was evaluated from the body composition by CT at the umbilicus and thigh levels. RESULTS: There was negative correlation between the insulinogenic index and age, but not between HOMA-IR and age. In relation to increasing age, the body composition changed toward a metabolically obese state, with increasing WHR, visceral fat area, VSR and VWR. Both the insulinogenic index and HOMA-IR were positively correlated with the anthropometric parameters. CONCLUSION: The age-associated deterioration in glucose tolerance may be due to decreases in both insulin secretion and insulin sensitivity from changes in body composition
Insulin Secretory Dysfunction in the Pathogenesis of Type 2 Diabetes in Koreans: A Minimal Model Analysis.
Sung Hoon Kim, Dong Jun Kim, Byung Wan Lee, In Ah Seo, Jae Hoon Chung, Young Ki Min, Myung Shik Lee, Kwang Won Kim, Moon Kyu Lee
Korean Diabetes J. 2003;27(5):414-419.   Published online October 1, 2003
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AbstractAbstract PDF
BACKGROUND
Type 2 diabetes is a complex, heterogeneous disorder, characterized by impairments in both insulin secretion and insulin action. This study was done to examine the significance of alterations in insulin sensitivity and beta-cell function in the pathogenesis of type 2 diabetes in Korean subjects with varying degrees of glucose intolerance. METHODS: Forty Korean subjects were studied, 12 with normal glucose tolerance (NGT), 14 with impaired glucose tolerance (IGT) and 14 with type 2 diabetes. An oral glucose tolerance test (OGTT) was performed on each subject. Insulin sensitivity (SI), glucose effectiveness (Sg), acute insulin response after intravenous glucose (AIRg) and the disposition index (DI= SI x AIRg) were measured by the insulin-modified, frequently sampled intravenous glucose tolerance test (FSIGT). RESULTS: Neither fasting serum insulin level nor SI was significantly different among the NGT, lGT and diabetes groups. Sg was significantly lower in the type 2 diabetes group than in the NGT group. The mean AIRg was blunted in the IGT and diabetes groups when compared with the NGT group. DI was more powerful in differentiating between NGT and IGT, compared to AIRg alone. CONCLUSION: These findings suggest that a defect in the compensatory insulin secretion might be more important than insulin resistance in the development of type 2 diabetes in Korean subjects.
Impairment of Insulin Secretion by Fat Overload in Rat Pancreatic Islets and Effects of Antioxidants.
Chul Hee Kim, Chan Hee Kim, Hyeong Kyu Park, Kyo Il Suh, Ki Up Lee
Korean Diabetes J. 2002;26(5):347-356.   Published online October 1, 2002
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AbstractAbstract PDF
BACKGROUND
It has recently been suggested that fat overload on pancreatic beta cells is responsible for the abnormal pattern of insulin secretion in type 2 diabetes mellitus. Antioxidant treatment was reported to preserve beta cell function in animal models of diabetes. This study was undertaken to examine the effects of various free fatty acids and triglyceride on insulin secretion in isolated rat pancreatic islets. In addition, we examined the effects of antioxidants. METHODS: Pancreatic islets of normal Sprague-Dawley rats were isolated by intraductal injection of collagenase and Ficoll-gradient centrifugation. The islets were treated with palmitat0e (C16:0), oleate (C18:1), linoleate (C18:2), and triglyceride emulsions (intralipid) for 72hours. Basal and glucose-stimulated insulin secretions were measured. The effects of the antioxidants, vitamin E, alpha-lipoic acid, and N-acetyl cysteine, were examined on the fat-induced change of insulin secretion. RESULTS: All of the free fatty acids and the triglyceride increased the basal insulin secretion. In contrast, insulin secretion stimulated by 27 mM glucose was significantly decreased after the treatment with free fatty acids or triglycerides. The antioxidant could not prevent the fat-induced inhibition of insulin secretion. CONCLUSION: These results show that various free fatty acids and triglyceride commonly cause defects in insulin secretion. However, we could not confirm the the hypothesis that increased oxidative stress may be involved in the pathogenesis of insulin secretory defect associated with fat overload.
Pospartum Assessment of Insulin Secretion and Sensitivity in Women with Gestational Diabetes Mellitus (GDM).
Eun Soon Hong, Hye Jin Lee, Young Sun Hong, Eon Ah Sung, Yeon Jin Jang
Korean Diabetes J. 2002;26(5):319-327.   Published online October 1, 2002
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AbstractAbstract PDF
BACKGROUND
Gestational diabetes mellitus (GDM) affects 2~4% of all pregnant women. Women with a history of GDM are at high risk of developing type 2 DM, in the future; with a cumulative incidence is 40~60%. Therefore, the assessment of insulin secretion and sensitivity in women with a history of GDM should help in the elucidation of some of the underlying defects of insulin secretion or action in the evolution of type 2 DM. This study was performed to evaluate the characteristics of insulin secretory capacity and sensitivity in women with gestational diabetes following child birth. METHODS: Oral glucose tolerance tests were carried out at 6~8 weeks postpartum in 22 women with a history of GDM, and 20 age and weight matched non- pregnant controls. Frequently sampled intravenous glucose tolerance test (FSIGT) were done at 10~14 weeks postpartm, and insulin secretion was measured as the acute insulin response to glucose (AIRg) and insulin sensitivity as minimal model derived sensitivity index (SI). AIRg*SI was used as an index for beta-cell function because AIRg can be modulated by SI. RESULTS: According to the results of OGTT, the subjects with a history of GDM were classified into 2 groups, one of normal glucose tolerance (postpartum-NGT) (n=11) and the other of an impaired glucose tolerance (postpartum-IGT)(n=11). There were no significant differences in WHR (waist to hip ratio), blood pressure, and serum lipid concentrations among the controls, postpartum-NGT and postpartum-IGT group. The fasting glucose level was significantly higher in the postpartum-IGT group compared to the postpartum-NGT and control groups (p<0.05). The fasting serum insulin level was significantly lower in the postpartum-NGT and -IGT groups than in the control group (p<0.05). The AIRg and AIRg*SI were significantly lower in the postpartum-NGT and -IGT groups compared to the control group (p<0.05), however the SI was lower in the postpartum-NGT and -IGT groups compared to the control group, but the difference did not reach statistical significance. The percentage of parental with history of type 2 diabetes was significantly greater in the postpartum-IGT group compared to the postpartum-NGT group (p<0.05). No significant predictive factors for subsequent IGT were found inform a logistic regression analysis. CONCLUSION: The insulin secretory capacity of women previously having suffered GDM was impaired, even though their glucose tolerance was restored to normal following child birth. Our results suggest that impaired insulin secretion may be a major path-ophysiological factor in the development of type 2 DM in women with a previous history of GDM.
Homeostasis Model Assessment In Korean Type 2 Diabetes Patients.
Hyun Ha Chang, Jin Woo Kim, Mee Suk Rhu, Cheol Young Park, Seung Joon Oh, Jeong Taek Woo, Sung Woon Kim, Young Seol Kim, Young Kil Choi
Korean Diabetes J. 2002;26(4):296-305.   Published online August 1, 2002
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AbstractAbstract PDF
BACKGROUND
Both insulin resistance and decreased insulin secretion have been known to be defects causing type 2 diabetes. However, decreased insulin secretion rather than insulin resistance has been suggested to be a more important factor in development of type 2 diabetes in Korea. Thus, we undertook this study to evaluate insulin resistance and beta cell function in Korean type 2 diabetes patients. METHODS: Retrospectively, we applied HOMA model to 1,233 type 2 diabetes pateints (575 males and 658 females) and assessed HOMA(beta cell) function and HOMA(IR). RESULTS: The HOMA(IR) of Korean male was 2.6 (0.05~39.53) and that of Korean female was 3.1 (0.04~53.54), and the HOMA(beta cell) of male was 22.3 (0.2~873.8)%, and that of female was 30.6 (0.37~1738.3)%. There was no significant difference. There was no significant correlation between HOMA(IR) and age and duration of diabetes, but there was significant correlation between HOMA(beta cell) and BMI, 0 min, 30 min insulin level and 0 min C-peptide level in oGTT. In the group of high HOMA(IR) than lower HOMA(IR), HOMA(beta cell) have more strong correlation with age at dignosis, BMI, duration of diabetes, FBS, 0 min and 60 min insulin, 0 min C-peptide and 24 hour urine C-peptide. CONCLUSION: In comparison with HOMA Model of San Antonio Heart Study, the HOMA(beta cell) and HOMA(IR) of Korean were lower, so the HOMA(beta cell) and HOMA(IR) may be different between ethnic groups. And further prospective analysis for the evaluation of insulin resistance and insulin secretion defect with HOMA model should be done in Korean type 2 diabeties.
Effects of Hydrogen Peroxide on Insulin Secretion in Rat Pancreatic Islets.
Chul Hee Kim, Chan Hee Kim, Hyeong Kyu Park, Kyo Il Suh, Ki Up Lee
Korean Diabetes J. 2002;26(4):265-273.   Published online August 1, 2002
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AbstractAbstract PDF
BACKGROUND
It has been hypothesized that reactive oxygen species (ROS) are involved in the progression of beta cell dysfunction in both type 1 and type 2 diabetes mellitus. On the other hand, recent evidence suggests that ROS might be an integral component of intracellular signaling. This study was undertaken to examine effects of hydrogen peroxide (H2O2) on insulin secretion by various secretagogues in isolated rat pancreatic islets. METHODS: Pancreatic islets from normal Sprague-Dawley rats were isolated by intraductal injection of collagenase and Ficoll-gradient centrifugation. Isolated islets were treated with H2O2 directly added to the culture media or continuously generated by glucose-glucose oxidase system for 24 hours. Insulin secretion stimulated by glucose, arginine, and KCl was measured by radioimmunoassay. RESULTS: Basal insulin secretion was increased after treatment with H2O2. Treatment with low concentration of H2O2 stimulated insulin secretion in response to 27 mM glucose. In contrast, insulin secretion stimulated by 27 mM glucose was significantly decreased after treatment with high concentrations of H2O2. Arginine- stimulated insulin secretion was increased by both low- and high concentrations of H2O2. Insulin secretion stimulated by KCl was not affected by treatment with H2O2. CONCLUSION: These results suggest that the effect of H2O2 is diverse according to its concentration and different insulin secretagogues. In particular, H2O2 has a dual action on glucose-induced insulin secretion. At low concentration, H2O2 can stimulate insulin secretion probably by acting on signaling pathway of stimulus- secretion coupling. In contrast, high concentrations of H2O2 impairs glucose- induced insulin secretion, probably by acting as an oxidative stress.
Effects of Antioxidants on Ethidium Bromide-induced Inhibition of Insulin Secretion in Rat Pancreatic Islets.
Chul Hee Kim, Chan Hee Kim, Hyeong Kyu Park, Kyo Il Suh, Ki Up Lee
Korean Diabetes J. 2002;26(3):179-187.   Published online June 1, 2002
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BACKGROUND
It was recently shown that mitochondrial function in pancreatic beta-cells is essential in nutrient-stimulated insulin secretion. The inhibition of mitochondrial DNA (mtDNA) transcription by ethidium bromide (EtBr) has been reported to suppress glucose-induced insulin secretion in beta-cell lines. This study was undertaken to examine the effects of EtBr on insulin secretion in isolated normal rat pancreatic islets, and to see whether antioxidants could protect the beta-cell function against the EtBr-induced impairment. METHODS: Pancreatic islets of normal Sprague-Dawley rats were isolated by intraductal injection of collagenase followed by Ficoll-gradient centrifugation. Isolated islets were treated with 0.2 +/- 2.0 microgram/mL of EtBr for 2 to 6 days, and the glucose-stimulated insulin secretion measured. The effects of the antioxidant, vitamin E and alpha-lipoic acid, on the EtBr-induced inhibition of insulin secretion were also examined. RESULTS: EtBr inhibited the basal and glucose-stimulated insulin secretion in normal rat pancreatic islets in a dose- and time-dependent manner. Vitamin E and alpha-lipoic acid prevented the EtBr-induced inhibition of insulin secretion. CONCLUSION: Our results show that antioxidant can protect normal rat pancreatic islets from the EtBr-induced inhibition of insulin secretion. This suggests that oxidative stress is involved in the pathogenesis of the insulin secretory defect associated with mitochondrial dysfunction.
Pancreatic beta-cell Function and Development in Male Offspring of Protein-Malnourished Rats.
Hyeong Kyu Park, Cheng Ji Jin, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee
Korean Diabetes J. 2002;26(1):21-30.   Published online February 1, 2002
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AbstractAbstract PDF
BACKGROUND
Nutritional deprivation of the fetus and infant may be associated with susceptibility to impaired glucose tolerance or type 2 diabetes in adult life. This association has been interpreted as a long-term effects of nutritional factors that reduce fetal growth and impair the development of tissues that regulate glucose metabolism. This study aimed to investigate the effect of protein malnutrition in a fetus and early life on the pancreatic beta-cell function and development. METHODS: Sprague-Dawley rats were fed a low-protein (8% casein) diet during pregnancy and lactation. Their male offspring were weaned onto either a control (18% casein) diet (recuperated group, R) or a low-protein diet (low-protein group, LP). The offspring of the rats fed control diet were weaned onto control diet (control group, C). Glucose tolerance tests and morphometry of the pancreas were performed to evaluate the pancreatic beta-cell function and development at the 25th week of age. RESULTS: Offspring of the protein-malnourished rats had a significantly lower body weights than the controls. The R and LP showed no major impairment in glucose tolerance, but the plasma insulin concentrations in the R (0.24+/-.03 nmol/L) and LP (0.28+/-.02 nmol/L) groups were lower at 20 min during IVGTT than the C (0.43+/-.05 nmol/L) groups. The areas under the curve for insulin (AUC insulin) during IVGTT were significantly lower in R and LP (0.39+/-.03 nmol/L/min, 0.43+/-.02 nmol/L/min) groups than the C (0.54+/-.03 nmol/L/min) group. In particular, the rats with fetal protein malnutrition showed severe impairment in late-phase insulin secretion to a glucose load. Both the pancreas weight and the proportion of the pancreas weight to the body weight were significantly lower in the R and LP groups than the C group. The proportion of beta-cells to pancreatic cells was lower in the LP (0.91+/-.14%) group than the C (2.19+/-.23%) and R (1.79+/-.25%) group. The relative beta-cell mass was significantly lower in the LP (by 62%) group that the C group. CONCLUSION: Rats with fetal protein malnutrition showed persistently impaired pancreatic beta-cell development and reduced insulin secretion capacity. These findings suggest that in utero protein malnutrition can contribute to the development of type 2 diabetes in adult life along with other deleterious environmental or genetic conditions.
The Combined Effects of Protein Malnutrition and Chronic Alcohol lntake on lnsulin Secretion and Sensitivity in Growing Rats.
Bong Soo Cha, Chul Woo Ahn, Hae II Lee, Yong Seok Yoon, Jae Kyeung Sung, Young Duk Song, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Kap Bum Huh
Korean Diabetes J. 2000;24(1):19-36.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
This investigation was performed to examine the combined effects of protein malnutrition and chronic moderate amount of alcohol intake on insulin secretory capacity and sensitivity in growing rats. METHODS: Weanling 4-week-old male Sprague-Dawley rats were fed low protein [5%, (wt/wt)] or control (C, 20%) diet from 4 to 12 weeks and alcohol (5g/kg/d) or saline gavage from 8 to 12 weeks. All rats were divided into the 4 groups according to different diet protocols: group 1 (protein-deficient alcohol rats), group II (protein-deficient saline rats), group III (protein-sufficient alcohol rats), and group IV (protein-sufficient saline or control rats), At the age of 12 weeks, we determined the insulin secretory capacity and sensitivity in the 4 different diet groups. RESULTS: The results are summarized as following: 1. Normal weight gain was nearly completely arrested in protein-deficient rats compared to control rats. In protein-sufficient rats, chronic alcohol intake decreased body weight gain. Pancreatic weight adjusted with body weight was not different among the 4 groups, but epididymal fat weight adjusted with body weight was decreased in group II compared to group IV. 2. Intraperitoneal glucose tolerance was improved in group I compared to the other groups. Insulin responses to glucose challenge were markedly decreased in group II compared to group IV, but not in group l. 3. Glucose disposal rate during euglycemic clamp test was diminished in group II compared to qroup IV, but there were no differences between group I and group I 3. Glycogen synthase activities of skeletal muscle after 2 hour hyperinsulinemic state were not different among the 4 groups. 4. There were no differences of reserved insulin content of whole pancreas adjusted with pancreas weight among the 4 groups. 5. In light microscopic findings of pancreatic islets, sizes of islets, islet cells and nuclei were decreased in protein-deficlent rats compared to control rats. However, the sizes of islet cells and nuclei were further decreased in group II compared to group l. CONCLUSION: These results suggest that impaired insulin secretion and decreased insulin sensitivity due to protein malnutrition can be restored by chronic, moderate amount of alcohol intake, but these beneficial effects may not be appeared in protein-sufficient state. Therefore, the chronic alcohol intake differently influences glucose metabolism according to individual nutritional status, and further studies for the effects of alcohol intake in lean diabetic patients are required to extrapolate these resuits in human.
Mechanism of the lnsulin Secretory Defect by Chronically Elevated Glucose Leveis in Pancreatic lslets: Depletion of lnsulin Content due to Hyperstimulation by Glucose.
Yeon Ah Sung, Young Sun Hong
Korean Diabetes J. 2000;24(1):1-9.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Type 2 diabetes is characterized by impaired insulin secretion and decreased insulin sensitivity, although the exact relationship between these two derangements during the development of the disease has not been fully established. Hyperglycemia per se impairs insulin secretion in pancreatic B-cell and the mechanism of impaired insulin by chronic hyperglycemia could be the clue to clarify pathogenesis of type 2 diabetes, and possibly identify the treatments. This study was performed to elucidate the mechanism of impairment of glucose induced insulin secretion by chronic hyperglycemia in pancreatic islets. METHODS: Pancreatic islets were isolated from Sprague-Dawley rats. After incubation of islets in high glucose (20mM) and low glucose (5mM) media for 10 days, glucose (16.7 mM) induced insulin secretion and insulin and DNA content in the islets were measured. Then subcellular distribution of low molecular and heterotrimeric G-proteins were assessed by ADP-ribosylation and radiolabeled GTP binding. RESULTS: 1) Glucose-induced insulin secretion of the islets cultured for 10 days in high glucose media was significantly lower when compared with that in islets cultured in low glucose media (p<0,05) 2) Subcellular distributions of low and heterotrimeric G-protein was not different in the islets cultured in low glucose when compared to those cultured in high glucose. 3) lnsulin content was significantly lower in the islets cultured in high glucose media compared with that in islets cultured in low glucose media (p<0.05) 4) DNA content was not significantly different between the islets cultured in low and high glucose media, and insulin content to DNA ratio was significantly lower in the islets cultured in high glucose media compared with that in islets cultured in low glucose media (p<0.05). CONCLUSION: Impaired insulin secretion to glucose in pancreatic islets exposed to high glucose is caused by depletion of insulin stores affer hyperstimulation.
Differential Effects of Palmitate and Docosahexaenoic acid on ATP-sensitive K+ Channel Activity of Pancreatic beta-cells.
Yong Woon Kim, Kyeung Oh Doh, Dae Kyu Song, Jae Hoon Bae, Won Kyun Park, Kyu Jang Won, Hyoung Woo Lee, Suck Kang Lee
Korean Diabetes J. 1999;23(6):768-776.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Elevated levels of free fatty acids markedly enhance insulin secretion. However, dietary polyunsaturated fatty supplementation decrease insulin secretion. The effects of different type of fatty acids on cultured pancreatic beta cell remain controversy. Therefore, the specific goal of this study was to confirm the effect of palmitate and docosahexaenoic acid (DHA) on pancreatic beta-cells. We measured ATP-sensitive K+ (KATP) channel activity by patch clamp technique. METHOD: Pancreatic beta-cells were isolated from male Sprague-Dawley rats and cultured on the cover glass in the culture media. KATP channel activity of pancreatic beta-cells were measured by the cell-attached mode of the patch clamp technique. We treated 30 micrometer of palmitate and DHA dissolved with 3% albumin solution. RESULT: 30 micrometer of palmitate inhibited KATP channel activity. Moreover, after additions of 5 and 10 mM glucose, additional and dose dependent inhibitory effects were revealed. However, 30 micrometer of DHA did not have these additional inhibitory effect treated with 5 and lOmM glucose. CONCLUSION: Palmitate as a saturated fatty acid inhibited activity of KATP channel and increased inhibitory effect of glucose on this channel activity, however, DHA as a polyunsaturated fatty acid attenuated inhibitory effect of glucose on this channel activity.
Role of Nitric Oxide on the Insulin Secretion of Rat Pancreas.
Moon Suk Nam, Sung Ki Kim, Seong Bin Hong, Yeo Joo Kim, Mi Rim Kim, Yong Seong Kim, Young Duk Song, Hyun Chul Lee, Kap Bum Huh
Korean Diabetes J. 1999;23(6):748-756.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Diabetes mellitus could occur when insulin secretion of pancreas is inadequate in response to blood glucose. The mechanisms on failure of pancreatic beta cell are still not known. Several recent experiments have reported that nitric oxide (NO) may be considered as a modulator of insulin secretion and impairment associated with the beta cell. The present study was purposed to investigate the role of nitric oxide on the secretion of insulin of rat pancreas in vivo and in vitro. METHODS: The plasma insulin and glucose were measured after intravenous injection of nitric oxide synthase (NOS) inhibitor (NG-nitro-L-arginine methyl. ester, L-NAME) in male rat. Insulin release was determmed during stimulation of NOS inhibitor and nitric oxide donor (hydroxylamine) in the isolated pancreatic islets. RESULT: 1. The insulin secretory response with L-arginine stimulation after injection of NOS inhibitor (L-NAME) in rat was increased resulting in mild hypoglycemia which recovered promptly. This showed that NO were related with L-arginine induced insulin secretion. 2. After isolation of pancreatic islet, 11,0 mM glucose induced insulin release was increased in culture media and L-arginine (1.0 mM) induced insulin release was also increased compared with control (6.72+/-0.66 vs. 3.48+/-0.42 prnol/islet/hour, p<0.05). 3. L-arginine induced insulin release was increased with L-NAME in the isolated rat pancreatic islets (12.5+/-1.38 vs, 7.23+/-0.93 ng/islet/ hour, p<0.05). 4. Glucose induced insulin release was progressively inhibited by NO donor hydroxylamine in the isolated rat pancreas islet (6.72+/-0.75 vs. 2.46+/-0.60 pmol/islet/hour p<0.05). CONCLUSION: These results strongly suggest that nitric oxide is a negative modulator of insulin release in normal rats induced by the nutrient secretagogues L-arginine and glucose in vivo and in vitro. Further investigation on the mechanism of nitric oxide in insulin secretory pathway will be necessary.
Insulin Secretion, Insulin Sensitivity and Body Fat Distribution Patterns in Patients with Impaired Glucose Tolerance.
Jin Hwa Lee, Yeon Ah Sung, Nan Ho Kyung, Yeon Jin Jang
Korean Diabetes J. 1999;23(5):647-660.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Type 2 diabetes mellitus(DM) is characterized by impaired insulin secretion and decreased insulin sensitivity, and often preceded by impaired glucose tolerance (IGT). To determine the relative importance of impaired insulin secretion and insulin resistance in development of type 2 DM, we evaluated body fat distribution patterns, insulin secretion and sensitivity in patients with IGT. METHODS: Thirty-six patients with IGT and age and weight matched twenty-four control subjects, were recruited from urban diabetes incidence cohort. Fasting serum glucose and insulin were measured. Body fat distribution pattern was assessed by waist to hip ratio (WHR), percent body fat and fat mass measured by bioelectrical impedence analyzer, and visceral to subcutaneous fat ratio (VSR) at the level of umbilicus using the computed tomography. Using insulin modified intravenous glucose tolerance test, insulin sensitivity was measured as minimal model derived sensitivity index (S(I)), and insulin secretion was measured as acute insulin response to glucose (AIR(g)) and beta-cell disposition index (AlR(g) X Sr). RESULT: l) In the patients with IGT, AIR(g)X S(I)(p<0.01) and area under the curve of insulin (AUC(I))(p<0.01) were significantly decreased compared with control subjects and age was greater than control subjects without statistical significance (p=0.17). 2) In the patients with IGT, body fat distribution patterns, indices of insulin secretion and sensitivity were not different according to the presence of family history of DM. AIR, and S(I) were negatively correlated in control subjects (r=-0.38, p=0.08) and the patients with IGT without family history of DM (r=-0.37, p=0.10), but not in the patients with IGT with family history of DM. 3) In the patients with IGT, indices of insulin secretion and sensitivity were not different according to body mass index (BMI). In both obese (BMI>=25 kg/m ) and non-obese (BMI<25 kg/m) patients with IGT, AIR(g)(p<0.05) and AIR(g) X S(I) were significantly decreased compared with control subjects (p<0.01). 4) In control subjects, age (p<0.05) and body fat mass (p<0.05) were significantly associated with AIR(g) X S(I) by multiple regression analysis. In the patients with IGT, body fat mass was significantly associated with AIR(g)(p<0.01) and AUC(I)(p<0.01), and BMI(p<0.01) was significantly associated with S(I). CONCLUSION: In patients with IGT, impaired insulin secretion was more prominent than decreased insulin sensitivity as compared with control subjects regardless of obesity and the presence of family history.
The Study of Alteration of Beta Cells in Pancreatic Islets, Glusoce Metabolism and Insulin Secretion in Low Dose Streptozotocin Indeced Type 2 Diabetic Rat Model.
Young Goo Shin, Hong Seung Kim, Mi Deok Lee, Young Uck Kim, Ho Suck Kang, Tae Sun Hwang, Choon Hee Chung
Korean Diabetes J. 1999;23(3):256-268.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Korean diabetes is different from western diabetes due to the racial differences in genetic factors and susceptability. It has recently been suggested that thrifty phenotype hypothesis is related to the recent increase in prevalence of Korean diabetes, but we have little evidence about that. We obtained basic materials in the animal model of type 2 diabetes mellitus and conducted a morphologic study of the beta cell change, insulin secreting capacity, and glucose metabolism. METHODS: To obtain the reference data of a non-insulin dependent diabetic animal model, we performed the intraperitoneal glucose tolerance test (IPGTT), hyperinsulinemic euglycemic clamp and immunobistochemical staining on the sacrificed pancreatic tissues on a Sprague-Dawley male rat into which streptozotocin (STZ) had been injected during the early neonatal period. The study groups consisted of a normal control group with citrate buffer injection, a group with injection of 50 ug STZ per kg of weight and a group with injection of 75 ug STZ per kg of weight. STZ was injected within 12 hours after birth. RESULTS: l. Although, STZ injected groups had lower body weight than the control group 7 weeks after birth, there were no differences during 14 weeks. 2. The IPGTT results showed that the average level of whole blood glucose concentration of the group with 50 ug STZ per kg of weight was higher than that of the control group at 7 and 14 weeks after birth. The mean serum insulin concentration of the 75 ug STZ per kg of weight injected group was lower than that of the control group at 7 weeks after birth, but it was higher than that of the control group at 14 weeks. 3. The hyperinsulinemic euglycemic clamp study showed that the average level of peripheral glucose disposal rate of the STZ injected groups was lower than the control group, but there were no differences in the study groups. 4. Pancreatic islet showed decreased beta cell mass and increased beta cell size in the STZ injected groups but the BrdU labelling index was not different between the control and study groups. CONCLUSION: STZ injection into neonatal Sprague-Dawley male rats may result in a diabetic status due to both decreased insulin secretion and increased insulin resistance, which gives us useful reference data for type 2 diabetes mellitus in the animal model.
Pathogenetic Heterogeneity of Type 2 Diabetes Mellitus in Korea.
Seok Won Park, Yong Seok Yun, Young Duk Song, Hyun Chul Lee, Kap Bum Huh
Korean Diabetes J. 1999;23(1):62-69.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Insulin resistance and insulin sec- retory dysfunction are considered as pathogenetic meehanisms leading to type 2 diabetes mellitus. In Korea, clinical features of type 2 diabetes are quite different from those of western countries. There are many non-obese patients and some even experienced considerable weight 1oss around the onset of diabetes mellitus. We investigated the insulin secretory function and in vivo insulin sensitivity in Korean patients with type 2 diabetes. METHODS: 38 patients with type 2 diabetes mellitus (age; 47.3+/-9.1 yrs) and 30 control subjects (age; 25.72.7 yrs) were included in this study. Type 2 diabetic subjects were further divided into obese (BMI >25, n=13) and non-obese (BMI<25, n=25) groups. Insulin secretory responses to the 75g aal gluxse loading and euglycemic hyperinsulinemic clamp test were performed on all subjects. RESULTS: Type 2 diabetic subjects had significantly lower serum insulin levels at 30 min of OGTT, regardless of their obesity, compared to the control subjects. Mean glucose disposal rates (M-values) were decreased by 36% in non-obese type 2 diabetic subjects and 58% in obese type 2 diahetic subjects compared to the control subjects. But, about half (12/25) of non-obese type 2 diabetic subjects and 30% (4/13) of obese type 2 diabetic subjects had normal insulin sensitivity, defined by 95% confidence interval of control subjects. Insulin sensitivity index (M-value) was correlated with BMI, WHR, fasting insulin, and HDL-cholesterol concentrations in type 2 diabetic subjects. CONCLUSION: In Korean type 2 diabetic subjects, impairment of early-phase insulin secretion may be an universal finding, but insulin resistance is observed in about 60% of subjects. This result suggest that there is pathogenetic heterogeneity of type 2 diabetes rnellitus in Korea.
The Role of Insulin Secretion and Insulin Resistance in the Development of Korean Type 2 Diabetes Mellitus.
Bong Nam Chae, Seong Kyu Lee, Eun Gyoung Hong, Yoon Sok Chung, Kwan Woo Lee, Hyeon Man Kim
Korean Diabetes J. 1998;22(4):491-503.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Impaired insulin secretinn, peripheral insulin resistance, a disproportionately elevated rate of hepatic glucose production and influence of inherited or enviromental factors contribute to the pathogenesis of type 2 diabetes mellitus(DM). But, which defect is primary is still controversial To determine whether insulin resistance or insulin deficiency is primary in the pathogenesis of type 2 DM, we studied normal glucose tolerant offsprings of type 2 diabetic patients. METHODS: 22 offsprings of type 2 diabetic patients with normal glucose tolerance, ranging in age from 20 to 40 years, and 17 control subjects in same age range who had no family history of diabetes, and 21 diabetic subjects were included. We performed 75 g oral glucose tolerance test, euglycemic hyper-insulinemic clamp test and hyperglycemic clamp test. RESULTS: With euglycemic clamp test, the values of peripheral insulin sensitivity, M, were 8.59+0.94 mg/kg/min in control group, 6.98+0.65 mg/kg/min in offspring group, and 5.19+0.89 mg/kg/min in diabetes group (P<0.05). Considering that lower limit of the normal range were 3.78 mg/kg/min in M and 3.10 mg/kg/min in M/I, the frequency of insulin resistance was 14.3% in the offspring group and 33.3 % in diabetes group. First and second phase insulin secretion during hyperglycemic clamp test were blunted in diabetes group. In the offspring group, first and second phase insulin secretion during hyperglycemic clamp test were increased greater than control group, though statistically insignificant. The mean first phase insulin secretion were 38.55+6.81 pU/mL in control group, 55.09+9.40 pU/mL in the offspring group and 6.02+0.98 pU/mL in diabetes group (P<0.05). The mean second phase insulin secretion were 65.11+15.5 pU/mL in control group, 90.25 + 11.9 pU/mL in the offspring group and 17.6 +2.71 pUmL in diabetes group(P<0,05). Considering that lower limit of the normal range were 19.5 pU/mL in the first phase insulin secretion and 26.1 pU/mL in the second phase insulin secretion, the frequency of impaired insulin secretion was 14.3 % in the offspring group and 100 % in diabetes group. There was an inverse relation between insulin resistance and insulin secretion in control subjects. But in the offspring group, this relation was absent. CONCLUSION: Our results show that both insulin resistance and impaired insulin secretion contribute to the development of type 2. DM in Koreans. In addifion, diabetic subjects had more severe impairment in insulin secretory capacity than insulin resistance.
Effects of Free Fatty Acid on Insulin Secretion in Cultured Rat Pancreatic Islets.
Hong Kyu Kim, Young Il Kim, Chul Hee Kim, Joong Yoel Park, Sung Kwan Hong, Jae Dam Lee, Ki Up Lee
Korean Diabetes J. 1997;21(4):381-387.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
It has been recently suggested that enhanced fat oxidation is responsible for the abnormal insulin secretory pattern in non-insulin-dependent diabetes mellitus. This study was undertaken to assess the effect of chronic exposure of pancreatic islets to free fatty acid on insulin secretion. METHODS: Rat pancreatic islets were cultured in various concentrations of glucose(5.5, 11, 27 mM) for 48 hrs with or without addition of free fatty acid(90 upM linoleic acid), and the basal and glucose-stimulated insulin secretion were measured. The effect of fatty acid oxidation inhibitor(2-bromopalmitate) was also tested. RESULTS: Islets cultured in high glucose concentrations showed a marked increase in basal insulin secretion. Free fatty acid stimulated the basal insulin secretion in islets cultured at 5.5 or 11 mM glucose, but no additional effect was seen in islets eultured at 27 mM glucose. In contrast, glucose-stimulated insulin secretion was decreased in islets cultured in high glucose media. Exposure to free fatty acid exerted an additive inhibitory effect on glucose-induced insulin secretion in islets cultured at 5.5 or 1 1 mM glucose, but not in islets cultured at 27M glucose, An inhibitor of fatty acid oxidation, 2-bromopalmitate, prevented the fatty acid-induced changes in both basal and glucosestimulated insulin secretion. CONCLUSION: These results showed that longterm exposure of pancreatic islets to free fatty acid altered the dynamics of insulin secretion, probably through a glucosefatty acid cycle.
The Changes in Insulin Secretion and GTPase Activity after the Exposure to High Glucose in Rat Pancreatic Islets.
Young Sun Hong, Yeon Ah Sung, Nan Ho Kyung
Korean Diabetes J. 2000;24(5):515-523.   Published online January 1, 2001
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AbstractAbstract
BACKGROUND
Type 2 diabetes mellitus is characterized by defective glucose- induced and glucose-potentiated insulin secretion. Chronic elevation of glucose levels are considered to be a cause of impaired insulin secretion. It has been suggested that such defects in insulin secretion can be related to the alteration in stimulus-secretion coupling. Recent studies have provided evidences for the existence of guanine nucleotide-binding protein (G protein), and the regulatory role of G protein and GTPase activity in stimulus-secretion coupling in pancreatic islets. This study was performed to determine whether the exposure to high glucose concentration alters GTPase activity with decreased insulin secretion in pancreatic islets isolated from normal rats. METHODS: Pancreatic islets isolated from normal Sprague-Dawley rats were incubated in high (20 mM) and low (5 mM) glucose concentration for 48 hours. After incubation, glucose (20 mM) induced insulin secretion was measured. Then subcellular fractions of islets by homogenization and differential centrifugation were obtained and glucose induced inhibition of GTPase activities in each fraction was measured. RESULTS: 1) After 48 hour exposure to 5 mM and 20 mM glucose, insulin secretion in response to 20 mM glucose were 134.4+/-16.8 fmol/10 islets/hr and 90.0+/-10.2 fmol/10 islets/hr, respectively. After the exposure to high glucose, glucose-induced insulin secretion significantly decreased (p<0.05). 2) In each subcellular fraction, there was no significant difference between the islets exposed to 5 mM and 20 mM glucose in the degree of inhibition of GTPase activities by high glucose. CONCLUSION: The exposure to high glucose for 48 hours decreased insulin secretion without any significant differences in the degree of inhibition of GTPase activities. This results suggest that impaired insulin secretion by high glucose is not associated with the change in GTPase activity.
Insulin Secretion and Insulin Sensitivity in Korean Subjects with Impaired Glucose Intolerance.
Dong Jun Kim, Jong Ryul Hahm, In Kyoung Jeong, Tae Young Yang, Eun Young Oh, Yoon Ho Choi, Jae Hoon Chung, Yong Ki Min, Myung Shik Lee, Moon Kyu Lee, Kwang Won Kim
Korean Diabetes J. 2000;24(3):356-364.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Although insulin resistance has been known to be a primary defect causing type 2 diabetes in Pima Indians and Caucasians. However, insulin secretory defect rather than insulin resistance has been speculated and demonstrated to be a more important factor in the development of type 2 diabetes in other ethnic groups. Thus, we undertook this study to investigate the initial abnormality of glucose intolerance in Korean subjects. METHODS: 374 Korean subjects were stratified according to the World Health Organization criteria (normal glucose tolerance [NGT], n = 128; impaired glucose tolerance [IGT], n=128; diabetes, n=118) and subdivided further into the two groups; non-obese (BMI < 25 kg/m2) and obese group (BMI 25 kg/m2). Insulinogenic index (the ratio of the increment of insulin to that of plasma glucose 30 min after glucose load) was used as an index of early-phase insulin secretion. AUC insulin (area under the insulin curve during OGTT) was used as an index of total insulin secretion. Insulin resistance was assessed by HOMA (R), the R value of the Homeostasis model. RESULTS: Insulinogenic index decreased significantly in IGT compared with that in NGT in both non-obese and obese groups, respectively. There was no significant difference in AUC insulin and HOMA (R) between NGT and IGT group. WhereasAUC insulin showed its peak level in the range of IGT (7.7~9.9 mmol/L), insulinogenic index showed the peak level in the range of NGT (5.6~7.7 mmol/lL and decreased progressively with increase of plasma glucose 120 min value. CONCLUSION: Early-phase insulin secretory defect might be the initial abnormality in the development of IGT from NGT in both non-obese and obese Korean subjects.
Diabetes Metab J : Diabetes & Metabolism Journal
© Korean Diabetes Association.
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