
pmid: 18706397
Effects of non-esterified fatty acids (FAs) are accentuated when applied together with elevated glucose through preferential use of glucose as fuel, which leads to decreased oxidation of FAs. We examined how over-expression of the mitochondrial FA transporter carnitine palmitoyltransferase 1 (CPT1) affects glucose-stimulated insulin secretion (GSIS), apoptosis and ER stress in INS-1E cells cultured in the presence of elevated levels of glucose and palmitate. INS-1E cells were infected with Tet-ON regulated adenovirus containing CPT1 and cultured for 48h in the presence of 0.5mM palmitate and 20mM glucose. Over-expressing CPT1 lowered basal insulin secretion in a dose-dependent manner thereby improving GSIS from INS-1E cells. Also, apoptosis was alleviated and ER-stress markers p-eIF2alpha and CHOP were decreased in cells over-expressing CPT1. We conclude that regulated over-expression of CPT1 is beneficial for glucolipotoxic beta-cells.
Carnitine O-Palmitoyltransferase, Eukaryotic Initiation Factor-2, Palmitates, Apoptosis, Fatty Acids, Nonesterified, Endoplasmic Reticulum, Adenoviridae, Cell Line, Rats, Glucose, Insulin-Secreting Cells, Insulin Secretion, Animals, Insulin, Transcription Factor CHOP
Carnitine O-Palmitoyltransferase, Eukaryotic Initiation Factor-2, Palmitates, Apoptosis, Fatty Acids, Nonesterified, Endoplasmic Reticulum, Adenoviridae, Cell Line, Rats, Glucose, Insulin-Secreting Cells, Insulin Secretion, Animals, Insulin, Transcription Factor CHOP
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