Abstract
Pancreatic β-cells secrete insulin when blood glucose levels become high. However, when β-cells are chronically exposed to hyperglycemia, their function gradually deteriorates. Although such phenomena are called as β-cell glucose toxicity, its molecular mechanism remained unclear. This manuscript describes the possible mechanism for such β-cell dysfunction. In the diabetic state, nuclear expression levels of pancreatic transcription factors PDX-1 and MafA are decreased. In addition, incretin receptor expression in β- cells is decreased, which is likely involved in the impairment of incretin effects in diabetes. Taken together, it is likely that down-regulation of pancreatic transcription factors and/or incretin receptors are involved in β-cell dysfunction observed in type 2 diabetes.
Keywords: Pancreatic β-cells, reactive oxygen species, PDX-1, MafA, GLP-1 receptor.
Current Diabetes Reviews
Title:Pancreatic β-cell Glucose Toxicity in Type 2 Diabetes Mellitus
Volume: 11 Issue: 1
Author(s): Hideaki Kaneto
Affiliation:
Keywords: Pancreatic β-cells, reactive oxygen species, PDX-1, MafA, GLP-1 receptor.
Abstract: Pancreatic β-cells secrete insulin when blood glucose levels become high. However, when β-cells are chronically exposed to hyperglycemia, their function gradually deteriorates. Although such phenomena are called as β-cell glucose toxicity, its molecular mechanism remained unclear. This manuscript describes the possible mechanism for such β-cell dysfunction. In the diabetic state, nuclear expression levels of pancreatic transcription factors PDX-1 and MafA are decreased. In addition, incretin receptor expression in β- cells is decreased, which is likely involved in the impairment of incretin effects in diabetes. Taken together, it is likely that down-regulation of pancreatic transcription factors and/or incretin receptors are involved in β-cell dysfunction observed in type 2 diabetes.
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Cite this article as:
Kaneto Hideaki, Pancreatic β-cell Glucose Toxicity in Type 2 Diabetes Mellitus, Current Diabetes Reviews 2015; 11 (1) . https://dx.doi.org/10.2174/1573399811666141216160217
DOI https://dx.doi.org/10.2174/1573399811666141216160217 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |
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