Diabetes & Metabolism Journal

Reviews

Guideline/Statement/Fact Sheet
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, Seon Mee Kang, Hyuk-Sang Kwon, Mi Kyung Kim, You-Bin Lee, Se Hee Min, Jung Hwan Park, Woo Je Lee, Bong-Soo Cha, Byung-Wan Lee; Diabetes Metab J. 2025;49(6):1155-1177. Published online November 1, 2025; DOI: https://doi.org/10.4093/dmj.2025.0978

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Abstract PDF Supplementary Material PubReader ePub: This Korean Diabetes Association (KDA) consensus statement bridges global evidence with the Korean clinical context, where large randomized and real-world data remain limited. Recommendations required ≥80% agreement by the committee of clinical practice guideline and approval by the board of directors. The statement comprises three domains: diabetes screening aligned with Korean epidemiology; pharmacologic management guided by pathophysiology and comorbidities; and a severity construct of “severe diabetes mellitus” that links complication-based staging with metabolic grading to match therapeutic intensity to disease complexity. Compared with prior KDA guidelines, this statement introduces substantive advances in three areas. First, screening recommendations are streamlined to emphasize risk-aligned, practical implementation rather than prescriptive test sequences. Second, pharmacologic management applies an individualized framework for drug selection that jointly considers pathophysiology and comorbidities. It operationalizes individualized selection by dominant pathophysiology (insulin resistance vs. insulin insufficiency) and coexisting conditions, and formalizes treatment dynamics—early combination, timely initiation of injectables, avoidance of overbasalization, and structured deintensification. It also prioritizes agents with proven cardiovascular and renal protection and elevates management of obesity and metabolic dysfunction-associated steatotic liver disease as central goals; clinically, insulin should be initiated promptly in hypercatabolic states or suspected islet failure, and technology-enabled care—including continuous glucose monitoring and automated insulin delivery—are integral across all stages. Third, the newly introduced severity construct underpins treatment-intensity decisions across domains without reiterating prescriptive algorithms. Collectively, these recommendations provide a coherent, context-appropriate framework for diabetes screening and management in Korea and identify priorities for future evidence generation.

Basic Research
Heterogeneity of Islet Cells during Embryogenesis and Differentiation: Shugo Sasaki, Takeshi Miyatsuka; Diabetes Metab J. 2023;47(2):173-184. Published online January 12, 2023; DOI: https://doi.org/10.4093/dmj.2022.0324

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Diabetes is caused by insufficient insulin secretion due to β-cell dysfunction and/or β-cell loss. Therefore, the restoration of functional β-cells by the induction of β-cell differentiation from embryonic stem (ES) and induced-pluripotent stem (iPS) cells, or from somatic non-β-cells, may be a promising curative therapy. To establish an efficient and feasible method for generating functional insulin-producing cells, comprehensive knowledge of pancreas development and β-cell differentiation, including the mechanisms driving cell fate decisions and endocrine cell maturation is crucial. Recent advances in single-cell RNA sequencing (scRNA-seq) technologies have opened a new era in pancreas development and diabetes research, leading to clarification of the detailed transcriptomes of individual insulin-producing cells. Such extensive high-resolution data enables the inference of developmental trajectories during cell transitions and gene regulatory networks. Additionally, advancements in stem cell research have not only enabled their immediate clinical application, but also has made it possible to observe the genetic dynamics of human cell development and maturation in a dish. In this review, we provide an overview of the heterogeneity of islet cells during embryogenesis and differentiation as demonstrated by scRNA-seq studies on the developing and adult pancreata, with implications for the future application of regenerative medicine for diabetes.

Citations

Citations to this article as recorded by

Pancreatic β-cell remodeling in health and aging: Lessons from rodents and humans
Radwan Darwish, Yasmine Alcibahy, Sangeeta Dhawan, Alexandra E. Butler, Abu Saleh Md Moin
Ageing Research Reviews.2025; 110: 102815. CrossRef
Single-cell RNA sequencing in studies of type 1 diabetes mellitus: modern state-of-the-art and technical peculiarities
Azat Vadimovich Abdullatypov, Olga Valentinovna Glushkova, Ekaterina Sergeevna Petriaikina, Viktor Pavlovich Bogdanov, Dmitry Vyacheslavovich Tabakov, Vasilii Eduardovich Akimov, Vladimir Sergeevich Yudin, Anton Arturovich Keskinov, Sergey Mikhailovich Yu
Frontiers in Endocrinology.2025;[Epub] CrossRef
Imeglimin enhances α-to-β reprograming mediated by PDX1 in β-cell ablated islets
Rei Fujishima, Tomomi Taguchi, Naoya Shimizu, Agena Suzuki, Wataru Hagiwara, Shiori Ito, Satomi Takebe, Mitsuko Inoue, Takeshi Miyatsuka
Biochemical and Biophysical Research Communications.2025; 790: 152886. CrossRef
Transcriptional and temporal heterogeneity of developing α cells revealed by single-cell RNA sequencing
Naoya Shimizu, Tomomi Taguchi, Miwa Himuro, Iichiro Shimomura, Francis C. Lynn, Hirotaka Watada, Shugo Sasaki, Takeshi Miyatsuka
Biochemical and Biophysical Research Communications.2025; 792: 152996. CrossRef
Investigation of the motif activity of transcription regulators in pancreatic β-like cell subpopulations differentiated from human induced pluripotent stem cells
Eric Leclerc, Mikhail Pachkov, Lisa Morisseau, Fumiya Tokito, Cecile Legallais, Rachid Jellali, Masaki Nishikawa, Amar Abderrahmani, Yasuyuki Sakai
Molecular Omics.2024; 20(10): 654. CrossRef
Newly discovered knowledge pertaining to glucagon and its clinical applications
Dan Kawamori, Shugo Sasaki
Journal of Diabetes Investigation.2023; 14(7): 829. CrossRef

Original Articles

Others
Influence of Maternal Diabetes on the Risk of Neurodevelopmental Disorders in Offspring in the Prenatal and Postnatal Periods: Verónica Perea, Xavier Urquizu, Maite Valverde, Marina Macias, Anna Carmona, Esther Esteve, Gemma Escribano, Nuria Pons, Oriol Giménez, Teresa Gironés, Andreu Simó-Servat, Andrea Domenech, Núria Alonso-Carril, Carme Quirós, Antonio J. Amor, Eva López, Maria José Barahona; Diabetes Metab J. 2022;46(6):912-922. Published online April 29, 2022; DOI: https://doi.org/10.4093/dmj.2021.0340

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Abstract PDF Supplementary Material PubReader ePub

Background
This study aimed to evaluate the influence of maternal diabetes in the risk of neurodevelopmental disorders in offspring in the prenatal and postnatal periods.
Methods
This cohort study included singleton gestational diabetes mellitus (GDM) pregnancies >22 weeks’ gestation with live newborns between 1991 and 2008. The control group was randomly selected and matched (1:2) for maternal age, weeks of gestation and birth year. Cox regression models estimated the effect of GDM on the risk of attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and maternal type 2 diabetes mellitus (T2DM). Moreover, interaction between maternal T2DM and GDM-ADHD relationship was evaluated.
Results
Children (n=3,123) were included (1,073 GDM; 2,050 control group). The median follow-up was 18.2 years (interquartile range, 14.2 to 22.3) (n=323 with ADHD, n=36 with ASD, and n=275 from women who developed T2DM). GDM exposure was associated with ADHD (hazard ratio [HR]_crude, 1.67; 95% confidence interval [CI], 1.33 to 2.07) (HR_adjusted, 1.64; 95% CI, 1.31 to 2.05). This association remained significant regardless of the treatment (diet or insulin) and diagnosis after 26 weeks of gestation. Children of mothers who developed T2DM presented higher rates of ADHD (14.2 vs. 10%, P=0.029). However, no interaction was found when T2DM was included in the GDM and ADHD models (P>0.05). GDM was not associated with an increased risk of ASD (HR_adjusted, 1.46; 95% CI, 0.74 to 2.84).
Conclusion
Prenatal exposure to GDM increases the risk of ADHD in offspring, regardless of GDM treatment complexity. However, postnatal exposure to maternal T2DM was not related to the development of ADHD.

Citations

Citations to this article as recorded by

Maternal diabetes during pregnancy and offspring's risk of autism spectrum disorder: A systematic review and meta-analysis
Mayra J. Garza-Martínez, José Á. Hernández-Mariano, Erika M. Hurtado-Salgado, Lea A. Cupul-Uicab
Journal of Psychiatric Research.2025; 182: 100. CrossRef
The association between maternal diabetes and the risk of attention deficit hyperactivity disorder in offspring: an updated systematic review and meta-analysis
Yitayish Damtie, Berihun Assefa Dachew, Getinet Ayano, Abay Woday Tadesse, Kim Betts, Rosa Alati
European Child & Adolescent Psychiatry.2025; 34(8): 2417. CrossRef
Research Progress on Short-Term and Long-Term Complications of Infants of Diabetic Mothers
桂婷冯
Advances in Clinical Medicine.2025; 15(03): 716. CrossRef
Gut–Brain Inflammatory Pathways in Attention-Deficit/Hyperactivity Disorder: The Role and Therapeutic Potential of Diet
Naomi Lewis, Jim Lagopoulos, Anthony Villani
Metabolites.2025; 15(5): 335. CrossRef
The association between maternal diabetes, antidiabetic medication use, and severe ADHD requiring inpatient care: A registry-based cohort study
Yitayish Damtie, Kim Betts, Berihun Assefa Dachew, Getinet Ayano, Rosa Alati
Journal of Psychosomatic Research.2025; 195: 112167. CrossRef
Gestational Diabetes Mellitus Model and its Pharmacological Validation
A. S. Solomina, K. S. Kachalov, A. V. Rodina, A. D. Durnev, L. G. Kolik
Journal Biomed.2025; 21(2): 58. CrossRef
“Risk of Autism Spectrum Disorder in Descendants of Women With Gestational Diabetes and Polycystic Ovary Syndrome: A Systematic Review and Meta‐Analysis”
Francisca Bravo‐Muñoz, Isidora Bustos, Diana Muñoz‐Fierro, Sofía San‐Martín, Catalina Tabilo, Macarena Véliz, Taide Zaror, Paulina Ormazabal, Nele Brusselaers, Romina Fornes
Autism Research.2025; 18(10): 1916. CrossRef
Gestational Diabetes and Obesity: Immediate and Late Sequelae for Offspring
Maria Kaza, George Paltoglou, Kalliopi Rodolaki, Konstantinos Kakleas, Spyridon Karanasios, Kyriaki Karavanaki
Children.2025; 12(9): 1263. CrossRef
Exploring the relationship between maternal carbohydrate quality and quantity during pregnancy and early childhood neurodevelopment: a prospective cohort study within the BiSC cohort
Laura Panisello, Javier Mateu-Fabregat, Nil Novau-Ferré, Nicolas Ayala-Aldana, Sara Bernardo-Castro, Muriel Ferrer, Pol Jiménez-Arenas, Elisa Llurba, Camille Lassale, María Dolores Gómez-Roig, Jesús Vioque, Sandra González-Palacios, Oren Contreras-Rodrígu
European Journal of Nutrition.2025;[Epub] CrossRef
Effects of a Diabetic Microenvironment on Neurodegeneration: Special Focus on Neurological Cells
Vishal Chavda, Dhananjay Yadav, Snehal Patel, Minseok Song
Brain Sciences.2024; 14(3): 284. CrossRef
Understanding the link between different types of maternal diabetes and the onset of autism spectrum disorders
Wenyu Shao, Yichun Su, Jiayin Liu, Yulong Liu, Jinghui Zhao, Xiaotang Fan
Diabetes & Metabolism.2024; 50(4): 101543. CrossRef
Tracing the influence of prenatal risk factors on the offspring retina: Focus on development and putative long‐term consequences
Filipa I. Baptista, António F. Ambrósio
European Journal of Clinical Investigation.2024;[Epub] CrossRef
Risk cycling in diabetes and autism spectrum disorder: a bidirectional Mendelian randomization study
Yunfeng Yu, Xinyu Yang, Gang Hu, Keke Tong, Jingyi Wu, Rong Yu
Frontiers in Endocrinology.2024;[Epub] CrossRef
Maternal Diabetes Deregulates the Expression of Mecp2 via miR-26b-5p in Mouse Embryonic Neural Stem Cells
Sukanya Shyamasundar, Seshadri Ramya, Deepika Kandilya, Dinesh Kumar Srinivasan, Boon Huat Bay, Suraiya Anjum Ansari, S Thameem Dheen
Cells.2023; 12(11): 1516. CrossRef
Evaluating the prospects of using gestational diabetes mellitus model to find means of pharmacological correction of the disorders in rat offspring
A. S. Solomina, A. V. Rodina, K. S. Kachalov, A. D. Zakharov, A. D. Durnev
Pharmacokinetics and Pharmacodynamics.2023; (2): 45. CrossRef
Hair and cord blood element levels and their relationship with air pollution, dietary intake, gestational diabetes mellitus, and infant neurodevelopment
Yin-Yin Xia, Jamie V. de Seymour, Xiao-Jia Yang, Lin-Wei Zhou, Yue Liu, Yang Yang, Kathryn L. Beck, Cathryn A. Conlon, Toby Mansell, Boris Novakovic, Richard Saffery, Ting-Li Han, Hua Zhang, Philip N. Baker
Clinical Nutrition.2023; 42(10): 1875. CrossRef
Role of Excessive Weight Gain During Gestation in the Risk of ADHD in Offspring of Women With Gestational Diabetes
Verónica Perea, Andreu Simó-Servat, Carmen Quirós, Nuria Alonso-Carril, Maite Valverde, Xavier Urquizu, Antonio J Amor, Eva López, Maria-José Barahona
The Journal of Clinical Endocrinology & Metabolism.2022; 107(10): e4203. CrossRef

Basic Research
MondoA Is Required for Normal Myogenesis and Regulation of the Skeletal Muscle Glycogen Content in Mice: Hui Ran, Yao Lu, Qi Zhang, Qiuyue Hu, Junmei Zhao, Kai Wang, Xuemei Tong, Qing Su; Diabetes Metab J. 2021;45(3):439-451. Published online May 18, 2020; DOI: https://doi.org/10.4093/dmj.2019.0212; Correction in: Diabetes Metab J 2021;45(5):797 Correction in: Diabetes Metab J 2025;49(2):331

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Abstract PDF Supplementary Material PubReader ePub

Background

Skeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear.

Methods

We generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle.

Results

MAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake.

Conclusion

MondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.

Citations

Citations to this article as recorded by

The Function of MondoA and ChREBP Nutrient—Sensing Factors in Metabolic Disease
Byungyong Ahn
International Journal of Molecular Sciences.2023; 24(10): 8811. CrossRef
Normal and Neoplastic Growth Suppression by the Extended Myc Network
Edward V. Prochownik, Huabo Wang
Cells.2022; 11(4): 747. CrossRef
The Role of Mondo Family Transcription Factors in Nutrient-Sensing and Obesity
Huiyi Ke, Yu Luan, Siming Wu, Yemin Zhu, Xuemei Tong
Frontiers in Endocrinology.2021;[Epub] CrossRef

Review

The Roles of Clusterin on Morphogenesis of Beta Cells During Pancreas Regeneration.: Seok Woo Hong, KC Ranjan, Song Lee, Yong Jae Shin, Bon Hong Min, In Sun Park; Korean Diabetes J. 2007;31(1):1-8. Published online January 1, 2007; DOI: https://doi.org/10.4093/jkda.2007.31.1.1

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Abstract PDF

Clusterin is a highly glycosylated heterodimeric glycoprotein that plays diverse biological roles in various organs. The secreted clusterin has been established as a major form of the protein that exerts diverse tissue effects. For instance, clusterin is known to act in cell protection through the actions of extra-cellular molecular chaperones. In the extracellular milieu, clusterin participates in specific interactions with a diverse array of native biological molecules including LRP-2 (Lipoprotein receptor-related protein 2, also known as gp330 or megalin), which is involved in ligand endocytosis at the surfaces of certain epithelia. Clusterin is expressed transiently in developing and differentiating endocrine pancreatic cells and might be involved in pancreas development. This transient expression of clusterin at specific time points of pancreas development and cell differentiation during pancreas regeneration implies that the protein is a regulatory factor for cytodifferentiation as well as for replication. A specific action of the clusterin in the reconstruction and remodeling of the endocrine pancreas has been demonstrated. It also strongly stimulates duct cell differentiation into insulin-secreting cells under in vitro culture conditions. Clusterin appears thus as a potent regulator of insulin cell morphogenesis.

Citations

Citations to this article as recorded by

Effect of African Mango (Irvingia gabonesis, IGOB 131^TM) Extract on Glucose Regulation in STZ-Induced Diabetes
Yejin Ha, Minhee Lee, Han Ol Kwon, Yoo-Hyun Lee
Journal of the Korean Society of Food Science and Nutrition.2015; 44(11): 1607. CrossRef

Original Articles

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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Abstract 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.

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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Abstract 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.

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