详细记录  
题名:Down-regulation of pancreatic transcription factors and incretin receptors in type 2 diabetes.
作者:KANETO H; MATSUOKA TA;
来源:World J Diabetes. 2013 Dec 15;4(6):263-269. [ IF= 0.00 ] ]
URL :10.4239/wjd.v4.i6.263
日期:20140217
摘要:Type 2 diabetes is one of the most prevalent and serious metabolic diseases.
Under diabetic conditions, chronic hyperglycemia and subsequent induction of
oxidative stress deteriorate pancreatic beta-cell function, which leads to the
aggravation of type 2 diabetes. Although such phenomena are well known as glucose
toxicity, its molecular mechanism remains unclear. In this review article, we
describe the possible molecular mechanism for beta-cell dysfunction found in type
2 diabetes, focusing on (1) oxidative stress, (2) pancreatic transcription
factors (PDX-1 and MafA) and (3) incretin receptors (GLP-1 and GIP receptors).
Under such conditions, nuclear expression levels of PDX-1 and MafA are decreased,
which leads to suppression of insulin biosynthesis and secretion. In addition,
expression levels of GLP-1 and GIP receptors are decreased, which likely
contributes to the impaired incretin effects found in diabetes. Taken together,
it is likely that down-regulation of pancreatic transcription factors (PDX-1 and
MafA) and down-regulation of incretin receptors (GLP-1 and GIP receptors)
explain, at least in part, the molecular mechanism for beta-cell dysfunction
found in type 2 diabetes.

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