The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.
Advanced Glycation End Products Inhibit Glucose-Stimulated Insulin Secretion through Nitric Oxide-Dependent Inhibition of Cytochrome c Oxidase and Adenosine Triphosphate Synthesis
Open accessAbstract
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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“AGEs also contribute to pancreatic 𝛽-cell dysfunction, another key component in the pathogenesis of T2DM.”
From The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction (2021) · cites this paper as [137]
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Cites
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Glucose-induced β cell production of IL-1β contributes to glucotoxicity in human pancreatic islets
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Glucose-induced β cell production of IL-1β contributes to glucotoxicity in human pancreatic islets
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Self-citationDiabetes and advanced glycation endproducts
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Self-citationA Lesson in Metabolic Regulation Inspired by the Glucokinase Glucose Sensor Paradigm
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Advanced Glycation End Products and Oxidative Stress in Type 2 Diabetes Mellitus
Nowotny, K., Jung, T., Höhn, A., Weber, D., & Grune, T. (2015) · Biomolecules · doi:10.3390/biom5010194 · Cited by 1,095
Giri, B., Dey, S., Das, T., Sarkar, M., Banerjee, J., & Dash, S. K. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.07.157 · Cited by 706
Advanced Glycation End Products (AGE) and Diabetes: Cause, Effect, or Both?
Vlassara, H., & Uribarri, J. (2014) · Current Diabetes Reports · doi:10.1007/s11892-013-0453-1 · Cited by 594
Self-citationFinch, C. E. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0909606106 · Cited by 417
Bao, H., Cao, J., Chen, M., Min, C., Chen, W., Chen, X., Chen, Y., Chen, Y., Chen, Y., Chen, Z., et al. (2023) · Science China Life Sciences · doi:10.1007/s11427-023-2305-0 · Cited by 402
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Metadata
- 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
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2009-02-26
- Volume
- 150
- Issue
- 6
- Pages
- 2569-2576
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- 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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