详细记录  
题名:B-cell translocation gene 2 positively regulates GLP-1-stimulated insulin secretion via induction of PDX-1 in pancreatic beta-cells.
作者:HWANG SL; KWON O; KIM SG; LEE IK; KIM YD;
来源:Exp Mol Med. 2013 May 24;45:e25. doi: 10.1038/emm.2013.47. [ IF= 0.00 ] ]
URL :10.1038/emm.2013.47
日期:20130606
摘要:Glucagon-like peptide-1 (GLP-1) is a potent glucoincretin hormone and an
important agent for the treatment of type 2 diabetes. Here we demonstrate that
B-cell translocation gene 2 (BTG2) is a crucial regulator in GLP-1-induced
insulin gene expression and insulin secretion via upregulation of pancreatic
duodenal homeobox-1 (PDX-1) in pancreatic beta-cells. GLP-1 treatment
significantly increased BTG2, PDX-1 and insulin gene expression in pancreatic
beta-cells. Notably, adenovirus-mediated overexpression of BTG2 significantly
elevated insulin secretion, as well as insulin and PDX-1 gene expression.
Physical interaction studies showed that BTG2 is associated with increased PDX-1
occupancy on the insulin gene promoter via a direct interaction with PDX-1.
Exendin-4 (Ex-4), a GLP-1 agonist, and GLP-1 in pancreatic beta-cells increased
insulin secretion through the BTG2-PDX-1-insulin pathway, which was blocked by
endogenous BTG2 knockdown using a BTG2 small interfering RNA knockdown system.
Finally, we revealed that Ex-4 and GLP-1 significantly elevated insulin secretion
via upregulation of the BTG2-PDX-1 axis in pancreatic islets, and this phenomenon
was abolished by endogenous BTG2 knockdown. Collectively, our current study
provides a novel molecular mechanism by which GLP-1 positively regulates insulin
gene expression via BTG2, suggesting that BTG2 has a key function in insulin
secretion in pancreatic beta-cells.

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