Chronic palmitate exposure inhibits AMPKα and decreases glucose-stimulated insulin secretion from β-cells: modulation by fenofibrate

摘要: Aim: Adenosine monophosphate-activated protein kinase (AMPK), a vital regulator of glucose metabolism, may affect insulin secretion in β-cells. However, the role AMPK β-cell lipotoxicity remains unclear. Fenofibrate has been reported to regulate lipid homeostasis and is involved pancreatic In present study, we aimed investigate effect palmitate on expression glucose-stimulated (GSIS) rat islets INS-1 β-cell, as well fenofibrate GSIS cells treated with palmitate. Methods: Isolated β-cells were without or for 48 h. The mRNA levels AMPKαisoforms measured by real-time PCR. Western blotting was used detect total AMPKα (T-AMPKα), phosphorylated (P-AMPKα), acetyl coenzyme A carboxylase (P-ACC). Insulin detected radioimmunoassay induced 20 mmol/L GSIS. Results: results showed that chronic exposure h inhibited AMPKα1 T-AMPKα levels, P-AMPKα P-ACC expressions dose-dependent manner. Accordingly, palmitate. Compared palmitate-treated cells, ameliorated these changes impaired exhibited significant elevation Conclusion: Our findings suggest reduction novel improving associated activation chronically exposed