详细记录  
题名:Glucagon-like Peptide-1 triggers protective pathways in pancreatic Beta-cells exposed to glycated serum.
作者:PUDDU A; SANGUINETI R; DURANTE A; NENCIONI A; MACH F; MONTECUCCO F; VIVIANI GL;
来源:Mediators Inflamm. 2013;2013:317120. doi: 10.1155/2013/317120. Epub 2013 Apr 29. [ IF= 0.00 ] ]
URL :10.1155/2013/317120
日期:20130430
摘要:Advanced glycation end products (AGEs) might play a pathophysiological role in
the development of diabetes and its complications. AGEs negatively affect
pancreatic beta-cell function and the expression of transcriptional factors
regulating insulin gene. Glucagon-like peptide-1 (GLP-1), an incretin hormone
that regulates glucose homeostasis, might counteract the harmful effects of AGEs
on the beta cells in culture. The aim of this study was to identify the
intracellular mechanisms underlying GLP-1-mediated protection from AGE-induced
detrimental activities in pancreatic beta cells. HIT-T15 cells were cultured for
5 days with glycated serum (GS, consisting in a pool of AGEs), in the presence or
absence of 10 nmol/L GLP-1. After evaluation of oxidative stress, we determined
the expression and subcellular localization of proteins involved in maintaining
redox balance and insulin gene expression, such as nuclear factor
erythroid-derived 2 (Nrf2), glutathione reductase, PDX-1, and MafA. Then, we
investigated proinsulin production. The results showed that GS increased
oxidative stress, reduced protein expression of all investigated factors through
proteasome activation, and decreased proinsulin content. Furthermore, GS reduced
ability of PDX-1 and MafA to bind DNA. Coincubation with GLP-1 reversed these
GS-mediated detrimental effects. In conclusion, GLP-1, protecting cells against
oxidants, triggers protective intercellular pathways in HIT-T15 cells exposed to
GS.

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