Glucagon-like peptide 1 protects INS-1E mitochondria against palmitate-mediated beta-cell dysfunction: a proteomic study.

摘要: Prolonged exposure to palmitate impairs insulin secretion and leads beta-cell death. Some evidence suggests that could induce these effects through defects in mitochondrial function. However, the mechanisms of lipotoxicity are not well understood. In particular, little is known about response induced-palmitate stress which glucagon-like peptide-1 (GLP-1) exerts its potential protective effect dysfunction. The aim this study was analyze protein expression profiles enriched preparations INS-1E beta-cells treated with presence absence GLP-1 using gel-based gel-free proteomic approaches. INS1E were incubated 0.5 mM for 24 h, 10 nM GLP-1, mitochondria isolated. Co-incubation palmitate-treated lines identified several responsive proteins from different functional classes indicating major changes ATP production, oxidative stress, apoptosis, lipid amino acid metabolism. Moreover, an interaction network analysis metabolites found be differentially expressed has been performed understand pathways involved activity at level. summary, our results provided a snapshot affected by treatment gave us information on role GLP-1.