Cited by 132Advanced Glycation End Products researchPancreatic function and diabetesDiabetes Treatment and Management

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Advanced Glycation End Products Inhibit Glucose-Stimulated Insulin Secretion through Nitric Oxide-Dependent Inhibition of Cytochrome c Oxidase and Adenosine Triphosphate Synthesis

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Zhao, Zhengshan, Zhao, Chunying, Zhang, Xu Hannah, Zheng, Feng, Cai, Weijing, Vlassara, Helen, Ma, Zhongmin Alex·2009·Endocrinology

DOI 10.1210/en.2008-1342PMC PMC2689792

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Abstract

Advanced glycation end products (AGEs) are implicated in diabetic complications. However, their role in β-cell dysfunction is less clear. In this study we examined the effects of AGEs on islet function in mice and in isolated islets. AGE-BSA or BSA was administered ip to normal mice twice a day for 2 wk. We showed that AGE-BSA-treated mice exhibited significantly higher glucose levels and lower insulin levels in response to glucose challenge than did BSA-treated mice, although there were no significant differences in insulin sensitivity and islet morphology between two groups. Glucose-stimulated insulin secretion by islets of the AGE-BSA-treated mice or AGE-BSA-treated normal islets was significantly lower than that by islets isolated from the BSA-treated mice or BSA-treated normal islets. Furthermore, AGE treatment of islet β-cells inhibited ATP production, and glimepiride, a sulfonylurea derivative, restored glucose-stimulated insulin secretion. Further investigation indicated that AGEs inhibited cytochrome c oxidase activity by inducing the expression of inducible nitric oxide synthase (iNOS). Blocking the formation of nitric oxide with an iNOS selective inhibitor aminoguanidine reversed the inhibitory effects of AGEs on ATP production and insulin secretion. We conclude that AGEs inhibit cytochrome c oxidase and ATP production, leading to the impairment of glucose-stimulated insulin secretion through iNOS-dependent nitric oxide production.

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Authors: Zhao, Z., Zhao, C., Zhang, X. H., Zheng, F., Cai, W., Vlassara, H., & Ma, Z. A.
Affiliations: Icahn School of Medicine at Mount Sinai (US)
Corresponding author: Zhao, Zhengshan
ORCID: Zhao, Zhengshan
Zhao, Chunying
Zhang, Xu Hannah
Zheng, Feng
Venue: Endocrinology
Publisher: The Endocrine Society
Published: 2009-02-26
Volume: 150
Issue: 6
Pages: 2569-2576
ISSN: 0013-7227 (ISSN-L)
1945-7170
DOI: 10.1210/en.2008-1342
PMC: PMC2689792
OpenAlex: W2081193499
Cited by: 132
References: 54
Citations by year: 2025: 4 · 2024: 4 · 2023: 7 · 2022: 6 · 2021: 6 · 2020: 8 · 2019: 5 · 2018: 7 · 2017: 5 · 2016: 11 · 2015: 6 · 2014: 13 · 2013: 17 · 2012: 12
FWCI: 7.03
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Endocrinology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: American Diabetes Association
National Institutes of Health
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK063076, R21DK074805, DK074805, DK063076)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords: advanced glycation end products, glucose-stimulated insulin secretion, beta-cell dysfunction, cytochrome c oxidase, nitric oxide, inducible nitric oxide synthase, ATP production, islet function, diabetes complications, aminoguanidine, sulfonylureas, AGE-BSA
MeSH terms: Insulin Secretion, Adenosine Triphosphate, Animals, Cells, Cultured, Electron Transport Complex IV, Diabetes Mellitus, Disease Models, Animal, Female, Glucose, Insulin, Male, Mice, Inbred C57BL, Nitric Oxide, Glycation End Products, Advanced, Insulin-Secreting Cells, Mice, Nitric Oxide Synthase Type II

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Advanced Glycation End Products Inhibit Glucose-Stimulated Insulin Secretion through Nitric Oxide-Dependent Inhibition of Cytochrome c Oxidase and Adenosine Triphosphate Synthesis

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