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Original Article
Basic Research
Article image
Role of SUMO-Specific Protease 2 in Leptin-Induced Fatty Acid Metabolism in White Adipocytes
Praise Chanmee Kim, Ji Seon Lee, Sung Soo Chung, Kyong Soo Park
Diabetes Metab J. 2023;47(3):382-393.   Published online March 6, 2023
DOI: https://doi.org/10.4093/dmj.2022.0156
  • 3,610 View
  • 163 Download
  • 1 Web of Science
  • 1 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background
Leptin is a 16-kDa fat-derived hormone with a primary role in controlling adipose tissue levels. Leptin increases fatty acid oxidation (FAO) acutely through adenosine monophosphate-activated protein kinase (AMPK) and on delay through the SUMO-specific protease 2 (SENP2)–peroxisome proliferator-activated receptor δ/γ (PPARδ/γ) pathway in skeletal muscle. Leptin also directly increases FAO and decreases lipogenesis in adipocytes; however, the mechanism behind these effects remains unknown. Here, we investigated the role of SENP2 in the regulation of fatty acid metabolism by leptin in adipocytes and white adipose tissues.
Methods
The effects of leptin mediated by SENP2 on fatty acid metabolism were tested by siRNA-mediated knockdown in 3T3-L1 adipocytes. The role of SENP2 was confirmed in vivo using adipocyte-specific Senp2 knockout (Senp2-aKO) mice. We revealed the molecular mechanism involved in the leptin-induced transcriptional regulation of carnitine palmitoyl transferase 1b (Cpt1b) and long-chain acyl-coenzyme A synthetase 1 (Acsl1) using transfection/reporter assays and chromatin immunoprecipitation.
Results
SENP2 mediated the increased expression of FAO-associated enzymes, CPT1b and ACSL1, which peaked 24 hours after leptin treatment in adipocytes. In contrast, leptin stimulated FAO through AMPK during the initial several hours after treatment. In white adipose tissues, FAO and mRNA levels of Cpt1b and Acsl1 were increased by 2-fold 24 hours after leptin injection in control mice but not in Senp2-aKO mice. Leptin increased PPARα binding to the Cpt1b and Acsl1 promoters in adipocytes through SENP2.
Conclusion
These results suggest that the SENP2-PPARα pathway plays an important role in leptin-induced FAO in white adipocytes.

Citations

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  • Intermittent cold stimulation affects energy metabolism and improves stress resistance in broiler heart
    Tingting Li, Haidong Wei, Shijie Zhang, Xiaotao Liu, Lu Xing, Yuanyuan Liu, Rixin Gong, Jianhong Li
    Poultry Science.2024; 103(1): 103190.     CrossRef
Short Communication
Basic Research
Article image
GPR40 Agonism Modulates Inflammatory Reactions in Vascular Endothelial Cells
Joo Won Kim, Eun Roh, Kyung Mook Choi, Hye Jin Yoo, Hwan-Jin Hwang, Sei Hyun Baik
Diabetes Metab J. 2022;46(3):506-511.   Published online January 24, 2022
DOI: https://doi.org/10.4093/dmj.2021.0092
  • 5,163 View
  • 232 Download
  • 8 Web of Science
  • 8 Crossref
AbstractAbstract PDFPubReader   ePub   
Endothelial dysfunction is strongly linked with inflammatory responses, which can impact cardiovascular disease. Recently, G protein-coupled receptor 40 (GPR40) has been investigated as a modulator of metabolic stress; however, the function of GPR40 in vascular endothelial cells has not been reported. We analyzed whether treatment of GPR40-specific agonists modulated the inflammatory responses in human umbilical vein endothelial cells (HUVECs). Treatment with LY2922470, a GPR40 agonist, significantly reduced lipopolysaccharide (LPS)-mediated nuclear factor-kappa B (NF-κB) phosphorylation and movement into the nucleus from the cytosol. However, treatment with another GPR40 agonist, TAK875, did not inhibit LPS-induced NF-κB activation. LPS treatment induced expression of adhesion molecules vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) and attachment of THP-1 cells to HUVECs, which were all decreased by LY2922470 but not TAK875. Our results showed that ligand-dependent agonism of GPR40 is a promising therapeutic target for overcoming inflammatory reactions in the endothelium.

Citations

Citations to this article as recorded by  
  • Synthetic GPR40/FFAR1 agonists: An exhaustive survey on the most recent chemical classes and their structure-activity relationships
    Abhik Paul, Sourin Nahar, Pankaj Nahata, Arnab Sarkar, Avik Maji, Ajeya Samanta, Sanmoy Karmakar, Tapan Kumar Maity
    European Journal of Medicinal Chemistry.2024; 264: 115990.     CrossRef
  • Metabolite-sensing GPCRs in rheumatoid arthritis
    Xuezhi Yang, Wankang Zhang, Luping Wang, Yingjie Zhao, Wei Wei
    Trends in Pharmacological Sciences.2024; 45(2): 118.     CrossRef
  • Aloe emodin promotes mucosal healing by modifying the differentiation fate of enteroendocrine cells via regulating cellular free fatty acid sensitivity
    Weilian Bao, Jiaren Lyu, Guize Feng, Linfeng Guo, Dian Zha, Keyuan You, Yang Liu, Haidong Li, Peng Du, Daofeng Chen, Xiaoyan Shen
    Acta Pharmaceutica Sinica B.2024;[Epub]     CrossRef
  • GPR40 deficiency worsens metabolic syndrome‐associated periodontitis in mice
    Yanchun Li, Zhongyang Lu, Cameron L. Kirkwood, Keith L. Kirkwood, Stephen A. Wank, Ai‐Jun Li, Maria F. Lopes‐Virella, Yan Huang
    Journal of Periodontal Research.2023; 58(3): 575.     CrossRef
  • Signaling pathways and intervention for therapy of type 2 diabetes mellitus
    Rong Cao, Huimin Tian, Yu Zhang, Geng Liu, Haixia Xu, Guocheng Rao, Yan Tian, Xianghui Fu
    MedComm.2023;[Epub]     CrossRef
  • G Protein-Coupled Receptor 40 Agonist LY2922470 Alleviates Ischemic-Stroke-Induced Acute Brain Injury and Functional Alterations in Mice
    Yingyu Lu, Wanlu Zhou, Qinghua Cui, Chunmei Cui
    International Journal of Molecular Sciences.2023; 24(15): 12244.     CrossRef
  • AM1638, a GPR40-Full Agonist, Inhibited Palmitate- Induced ROS Production and Endoplasmic Reticulum Stress, Enhancing HUVEC Viability in an NRF2-Dependent Manner
    Hwan-Jin Hwang, Joo Won Kim, SukHwan Yun, Min Jeong Park, Eyun Song, Sooyeon Jang, Ahreum Jang, Kyung Mook Choi, Sei Hyun Baik, Hye Jin Yoo
    Endocrinology and Metabolism.2023; 38(6): 760.     CrossRef
  • Learn from failures and stay hopeful to GPR40, a GPCR target with robust efficacy, for therapy of metabolic disorders
    Hong-Ping Guan, Yusheng Xiong
    Frontiers in Pharmacology.2022;[Epub]     CrossRef
Original Article
Genetics
Article image
Enhancer-Gene Interaction Analyses Identified the Epidermal Growth Factor Receptor as a Susceptibility Gene for Type 2 Diabetes Mellitus
Yang Yang, Shi Yao, Jing-Miao Ding, Wei Chen, Yan Guo
Diabetes Metab J. 2021;45(2):241-250.   Published online June 10, 2020
DOI: https://doi.org/10.4093/dmj.2019.0204
  • 6,299 View
  • 104 Download
  • 4 Web of Science
  • 5 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background

Genetic interactions are known to play an important role in the missing heritability problem for type 2 diabetes mellitus (T2DM). Interactions between enhancers and their target genes play important roles in gene regulation and disease pathogenesis. In the present study, we aimed to identify genetic interactions between enhancers and their target genes associated with T2DM.

Methods

We performed genetic interaction analyses of enhancers and protein-coding genes for T2DM in 2,696 T2DM patients and 3,548 controls of European ancestry. A linear regression model was used to identify single nucleotide polymorphism (SNP) pairs that could affect the expression of the protein-coding genes. Differential expression analyses were used to identify differentially expressed susceptibility genes in diabetic and nondiabetic subjects.

Results

We identified one SNP pair, rs4947941×rs7785013, significantly associated with T2DM (combined P=4.84×10−10). The SNP rs4947941 was annotated as an enhancer, and rs7785013 was located in the epidermal growth factor receptor (EGFR) gene. This SNP pair was significantly associated with EGFR expression in the pancreas (P=0.033), and the minor allele “A” of rs7785013 decreased EGFR gene expression and the risk of T2DM with an increase in the dosage of “T” of rs4947941. EGFR expression was significantly upregulated in T2DM patients, which was consistent with the effect of rs4947941×rs7785013 on T2DM and EGFR expression. A functional validation study using the Mouse Genome Informatics (MGI) database showed that EGFR was associated with diabetes-relevant phenotypes.

Conclusion

Genetic interaction analyses of enhancers and protein-coding genes suggested that EGFR may be a novel susceptibility gene for T2DM.

Citations

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  • Hypoglycemic Activity of Rice Resistant-Starch Metabolites: A Mechanistic Network Pharmacology and In Vitro Approach
    Jianing Ren, Jing Dai, Yue Chen, Zhenzhen Wang, Ruyi Sha, Jianwei Mao, Yangchen Mao
    Metabolites.2024; 14(4): 224.     CrossRef
  • Genome-Wide Epistasis Study of Cerebrospinal Fluid Hyperphosphorylated Tau in ADNI Cohort
    Dandan Chen, Jin Li, Hongwei Liu, Xiaolong Liu, Chenghao Zhang, Haoran Luo, Yiming Wei, Yang Xi, Hong Liang, Qiushi Zhang
    Genes.2023; 14(7): 1322.     CrossRef
  • Investigation of the mechanism of Shen Qi Wan prescription in the treatment of T2DM via network pharmacology and molecular docking
    Piaopiao Zhao, Xiaoxiao Zhang, Yuning Gong, Weihua Li, Zengrui Wu, Yun Tang, Guixia Liu
    In Silico Pharmacology.2022;[Epub]     CrossRef
  • The Role of the Epidermal Growth Factor Receptor in Diabetic Kidney Disease
    Raymond C. Harris
    Cells.2022; 11(21): 3416.     CrossRef
  • Co-expression Network Revealed Roles of RNA m6A Methylation in Human β-Cell of Type 2 Diabetes Mellitus
    Cong Chen, Qing Xiang, Weilin Liu, Shengxiang Liang, Minguang Yang, Jing Tao
    Frontiers in Cell and Developmental Biology.2021;[Epub]     CrossRef
Review
Drug/Regimen
Fibrates Revisited: Potential Role in Cardiovascular Risk Reduction
Nam Hoon Kim, Sin Gon Kim
Diabetes Metab J. 2020;44(2):213-221.   Published online April 23, 2020
DOI: https://doi.org/10.4093/dmj.2020.0001
  • 8,026 View
  • 324 Download
  • 45 Web of Science
  • 44 Crossref
AbstractAbstract PDFPubReader   

Fibrates, peroxisome proliferator-activated receptor-α agonists, are potent lipid-modifying drugs. Their main effects are reduction of triglycerides and increase in high-density lipoprotein levels. Several randomized controlled trials have not demonstrated their benefits on cardiovascular risk reduction, especially as an “add on” to statin therapy. However, subsequent analyses by major clinical trials, meta-analyses, and real-world evidence have proposed their potential in specific patient populations with atherogenic dyslipidemia and metabolic syndrome. Here, we have reviewed and discussed the accumulated data on fibrates to understand their current status in cardiovascular risk management.

Citations

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  • Role of PPARα in inflammatory response of C2C12 myotubes
    Yuki Shimizu, Keiko Hamada, Tingting Guo, Chie Hasegawa, Yusuke Kuga, Katsushi Takeda, Takashi Yagi, Hiroyuki Koyama, Hiroshi Takagi, Daisuke Aotani, Hiromi Kataoka, Tomohiro Tanaka
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    Dimitris Kounatidis, Natalia G. Vallianou, Aikaterini Poulaki, Angelos Evangelopoulos, Fotis Panagopoulos, Theodora Stratigou, Eleni Geladari, Irene Karampela, Maria Dalamaga
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  • Role of Fenofibrate Use in Dyslipidemia and Related Comorbidities in the Asian Population: A Narrative Review
    Chaicharn Deerochanawong, Sin Gon Kim, Yu-Cheng Chang
    Diabetes & Metabolism Journal.2024; 48(2): 184.     CrossRef
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    Minjun Liao, Xueke He, Yangyang Zhou, Weiqiang Peng, Xiao-Mei Zhao, Miao Jiang
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  • Onion Polyphenols as Multi-Target-Directed Ligands in MASLD: A Preliminary Molecular Docking Study
    Maria Rosaria Paravati, Anna Caterina Procopio, Maja Milanović, Giuseppe Guido Maria Scarlata, Nataša Milošević, Maja Ružić, Nataša Milić, Ludovico Abenavoli
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    Katarina Lalić, Nataša Rajković, Ljiljana Popović, Sandra Singh-Lukač, Iva Rasulić, Ana Petakov, Milica Krstić, Marija Mitrović
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    Molecular Metabolism.2023; 69: 101685.     CrossRef
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  • Molecular mechanisms and therapeutic perspectives of peroxisome proliferator‐activated receptor α agonists in cardiovascular health and disease
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  • Effective, disease-modifying, clinical approaches to patients with mild-to-moderate hypertriglyceridaemia
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    The Lancet Diabetes & Endocrinology.2022; 10(2): 142.     CrossRef
  • Effects of Alirocumab on Triglyceride Metabolism: A Fat-Tolerance Test and Nuclear Magnetic Resonance Spectroscopy Study
    Thomas Metzner, Deborah R. Leitner, Karin Mellitzer, Andrea Beck, Harald Sourij, Tatjana Stojakovic, Gernot Reishofer, Winfried März, Ulf Landmesser, Hubert Scharnagl, Hermann Toplak, Günther Silbernagel
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Original Article
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
  • 6,557 View
  • 185 Download
  • 7 Web of Science
  • 6 Crossref
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.

Citations

Citations to this article as recorded by  
  • N6-methylation of RNA-bound adenosine regulator HNRNPC promotes vascular endothelial dysfunction in type 2 diabetes mellitus by activating the PSEN1-mediated Notch pathway
    Ying Cai, Tao Chen, Mingzhu Wang, Lihua Deng, Cui Li, Siqian Fu, Kangling Xie
    Diabetes Research and Clinical Practice.2023; 197: 110261.     CrossRef
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    Yunqian Yao, Ling Wei, Zhenhua Chen, Hao Li, Jiao Qi, Qingfeng Wu, Xingtao Zhou, Yi Lu, Xiangjia Zhu
    Cell Proliferation.2023;[Epub]     CrossRef
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    Yu‐Huan Peng, Ping Wang, Xiao‐Qun He, Ming‐Zhao Hong, Feng Liu
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  • Genome-Wide Meta-analysis Identifies Genetic Variants Associated With Glycemic Response to Sulfonylureas
    Adem Y. Dawed, Sook Wah Yee, Kaixin Zhou, Nienke van Leeuwen, Yanfei Zhang, Moneeza K. Siddiqui, Amy Etheridge, Federico Innocenti, Fei Xu, Josephine H. Li, Joline W. Beulens, Amber A. van der Heijden, Roderick C. Slieker, Yu-Chuan Chang, Josep M. Mercade
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Reviews
Obesity and Metabolic Syndrome
Understanding Bile Acid Signaling in Diabetes: From Pathophysiology to Therapeutic Targets
Jessica M. Ferrell, John Y. L. Chiang
Diabetes Metab J. 2019;43(3):257-272.   Published online June 13, 2019
DOI: https://doi.org/10.4093/dmj.2019.0043
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AbstractAbstract PDFPubReader   

Diabetes and obesity have reached an epidemic status worldwide. Diabetes increases the risk for cardiovascular disease and non-alcoholic fatty liver disease. Primary bile acids are synthesized in hepatocytes and are transformed to secondary bile acids in the intestine by gut bacteria. Bile acids are nutrient sensors and metabolic integrators that regulate lipid, glucose, and energy homeostasis by activating nuclear farnesoid X receptor and membrane Takeda G protein-coupled receptor 5. Bile acids control gut bacteria overgrowth, species population, and protect the integrity of the intestinal barrier. Gut bacteria, in turn, control circulating bile acid composition and pool size. Dysregulation of bile acid homeostasis and dysbiosis causes diabetes and obesity. Targeting bile acid signaling and the gut microbiome have therapeutic potential for treating diabetes, obesity, and non-alcoholic fatty liver disease.

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Pathophysiology
Nuclear Receptors Resolve Endoplasmic Reticulum Stress to Improve Hepatic Insulin Resistance
Jae Man Lee
Diabetes Metab J. 2017;41(1):10-19.   Published online February 16, 2017
DOI: https://doi.org/10.4093/dmj.2017.41.1.10
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AbstractAbstract PDFPubReader   

Chronic endoplasmic reticulum (ER) stress culminating in proteotoxicity contributes to the development of insulin resistance and progression to type 2 diabetes mellitus. Pharmacologic interventions targeting several different nuclear receptors have emerged as potential treatments for insulin resistance. The mechanistic basis for these antidiabetic effects has primarily been attributed to multiple metabolic and inflammatory functions. Here we review recent advances in our understanding of the association of ER stress with insulin resistance and the role of nuclear receptors in promoting ER stress resolution and improving insulin resistance in the liver.

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Interrelationships between the Retinal Neuroglia and Vasculature in Diabetes
Timothy S. Kern
Diabetes Metab J. 2014;38(3):163-170.   Published online June 17, 2014
DOI: https://doi.org/10.4093/dmj.2014.38.3.163
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AbstractAbstract PDFPubReader   

For years, diabetic retinopathy has been defined based on vascular lesions, and neural abnormalities were not regarded as important. This review summarizes evidence that the neural retina has important effects on the retinal vasculature under normal conditions, and the interaction between the retinal neuroglial cells and vascular function is altered in diabetes. Importantly, new evidence raises a possibility that abnormalities within retinal neuroglial cells (notably photoreceptors) might actually be causing or initiating the vascular disease in diabetic retinopathy.

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Targeting the Peroxisome Proliferator-Activated Receptor-γ to Counter the Inflammatory Milieu in Obesity
Cesar Corzo, Patrick R. Griffin
Diabetes Metab J. 2013;37(6):395-403.   Published online December 12, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.6.395
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AbstractAbstract PDFPubReader   

Adipose tissue, which was once viewed as a simple organ for storage of triglycerides, is now considered an important endocrine organ. Abnormal adipose tissue mass is associated with defects in endocrine and metabolic functions which are the underlying causes of the metabolic syndrome. Many adipokines, hormones secreted by adipose tissue, regulate cells from the immune system. Interestingly, most of these adipokines are proinflammatory mediators, which increase dramatically in the obese state and are believed to be involved in the pathogenesis of insulin resistance. Drugs that target peroxisome proliferator-activated receptor-γ have been shown to possess anti-inflammatory effects in animal models of diabetes. These findings, and the link between inflammation and the metabolic syndrome, will be reviewed here.

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Regulation of Muscle Pyruvate Dehydrogenase Complex in Insulin Resistance: Effects of Exercise and Dichloroacetate
Dumitru Constantin-Teodosiu
Diabetes Metab J. 2013;37(5):301-314.   Published online October 17, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.5.301
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AbstractAbstract PDFPubReader   

Since the mitochondrial pyruvate dehydrogenase complex (PDC) controls the rate of carbohydrate oxidation, impairment of PDC activity mediated by high-fat intake has been advocated as a causative factor for the skeletal muscle insulin resistance, metabolic syndrome, and the onset of type 2 diabetes (T2D). There are also situations where muscle insulin resistance can occur independently from high-fat dietary intake such as sepsis, inflammation, or drug administration though they all may share the same underlying mechanism, i.e., via activation of forkhead box family of transcription factors, and to a lower extent via peroxisome proliferator-activated receptors. The main feature of T2D is a chronic elevation in blood glucose levels. Chronic systemic hyperglycaemia is toxic and can lead to cellular dysfunction that may become irreversible over time due to deterioration of the pericyte cell's ability to provide vascular stability and control to endothelial proliferation. Therefore, it may not be surprising that T2D's complications are mainly macrovascular and microvascular related, i.e., neuropathy, retinopathy, nephropathy, coronary artery, and peripheral vascular diseases. However, life style intervention such as exercise, which is the most potent physiological activator of muscle PDC, along with pharmacological intervention such as administration of dichloroacetate or L-carnitine can prove to be viable strategies for treating muscle insulin resistance in obesity and T2D as they can potentially restore whole body glucose disposal.

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Transcriptional Regulation of Pyruvate Dehydrogenase Kinase
Ji Yun Jeong, Nam Ho Jeoung, Keun-Gyu Park, In-Kyu Lee
Diabetes Metab J. 2012;36(5):328-335.   Published online October 18, 2012
DOI: https://doi.org/10.4093/dmj.2012.36.5.328
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AbstractAbstract PDFPubReader   

The pyruvate dehydrogenase complex (PDC) activity is crucial to maintains blood glucose and ATP levels, which largely depends on the phosphorylation status by pyruvate dehydrogenase kinase (PDK) isoenzymes. Although it has been reported that PDC is phosphorylated and inactivated by PDK2 and PDK4 in metabolically active tissues including liver, skeletal muscle, heart, and kidney during starvation and diabetes, the precise mechanisms by which expression of PDK2 and PDK4 are transcriptionally regulated still remains unclear. Insulin represses the expression of PDK2 and PDK4 via phosphorylation of FOXO through PI3K/Akt signaling pathway. Several nuclear hormone receptors activated due to fasting or increased fat supply, including peroxisome proliferator-activated receptors, glucocorticoid receptors, estrogen-related receptors, and thyroid hormone receptors, also participate in the up-regulation of PDK2 and PDK4; however, the endogenous ligands that bind those nuclear receptors have not been identified. It has been recently suggested that growth hormone, adiponectin, epinephrine, and rosiglitazone also control the expression of PDK4 in tissue-specific manners. In this review, we discuss several factors involved in the expressional regulation of PDK2 and PDK4, and introduce current studies aimed at providing a better understanding of the molecular mechanisms that underlie the development of metabolic diseases such as diabetes.

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Original Article
Effects of Sulfonylureas on Peroxisome Proliferator-Activated Receptor γ Activity and on Glucose Uptake by Thiazolidinediones
Kyeong Won Lee, Yun Hyi Ku, Min Kim, Byung Yong Ahn, Sung Soo Chung, Kyong Soo Park
Diabetes Metab J. 2011;35(4):340-347.   Published online August 31, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.4.340
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AbstractAbstract PDFPubReader   
Background

Sulfonylurea primarily stimulates insulin secretion by binding to its receptor on the pancreatic β-cells. Recent studies have suggested that sulfonylureas induce insulin sensitivity through peroxisome proliferator-activated receptor γ (PPARγ), one of the nuclear receptors. In this study, we investigated the effects of sulfonylurea on PPARγ transcriptional activity and on the glucose uptake via PPARγ.

Methods

Transcription reporter assays using Cos7 cells were performed to determine if specific sulfonylureas stimulate PPARγ transactivation. Glimepiride, gliquidone, and glipizide (1 to 500 µM) were used as treatment, and rosiglitazone at 1 and 10 µM was used as a control. The effects of sulfonylurea and rosiglitazone treatments on the transcriptional activity of endogenous PPARγ were observed. In addition, 3T3-L1 adipocytes were treated with rosiglitazone (10 µM), glimepiride (100 µM) or both to verify the effect of glimepiride on rosiglitazone-induced glucose uptake.

Results

Sulfonylureas, including glimepiride, gliquidone and glipizide, increased PPARγ transcriptional activity, gliquidone being the most potent PPARγ agonist. However, no additive effects were observed in the presence of rosiglitazone. When rosiglitazone was co-treated with glimepiride, PPARγ transcriptional activity and glucose uptake were reduced compared to those after treatment with rosiglitazone alone. This competitive effect of glimepiride was observed only at high concentrations that are not achieved with clinical doses.

Conclusion

Sulfonylureas like glimepiride, gliquidone and glipizide increased the transcriptional activity of PPARγ. Also, glimepiride was able to reduce the effect of rosiglitazone on PPARγ agonistic activity and glucose uptake. However, the competitive effect does not seem to occur at clinically feasible concentrations.

Citations

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Review
Functional and Mechanistic Integration of Infection and the Metabolic Syndrome
Peter Sommer, Gary Sweeney
Korean Diabetes J. 2010;34(2):71-76.   Published online April 30, 2010
DOI: https://doi.org/10.4093/kdj.2010.34.2.71
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AbstractAbstract PDFPubReader   

The metabolic syndrome refers to a well defined group of risk factors, including central obesity and inflammation, for the development of diabetes and cardiovascular disease. Interestingly, many studies have recently led to the emergence of somewhat unexpected relationships between several infectious diseases and various aspects of the metabolic syndrome. Our understanding of the mechanisms underlying these interactions is also rapidly developing and some of these are summarized in this article. We will focus first on bacterial infection, and most notably the role of gut microbiota in regulaton of both obesity and inflammation. In particular, we focus on the role of inflammasomes and propose that understanding the role of Toll-like receptors and Nod-like receptors in the pathogenesis of inflammatory disorders with or without infection may provide novel targets for prevention and/or treatment of associated diseases. Secondly, chronic bacterial or viral infection and emerging links with metabolism will be reviewed. Finally, consideratons of biomarkers for metabolic syndrome, in particular lipocalin-2, and their link with infection will be discussed.

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