Palmitate activates AMP-activated protein kinase and regulates insulin secretion from β cells

AMP-activated protein kinase (AMPK) is an energy sensor that regulates cellular metabolism. Changes in AMPK activity contribute to the regulation of insulin secretion. Epidemiological evidence links the ingestion of saturated fatty acid with hyperinsulinemia. The aim of the present study was to examine the effects of palmitate on β cell AMPK activity and insulin secretion. Isolated rat islets and MIN6 β cells were treated acutely (5-60 min) or chronically (24 h) with palmitate. Insulin secretion, AMPK and acetyl CoA carboxylase phosphorylation were assessed. The acute effects of palmitate included AMPK activation and augmentation in insulin secretion. Activation of AMPK by 24 h pretreatment with palmitate suppressed glucose-stimulated insulin secretion, but not the response of insulin secretion to combined stimuli of glucose and palmitate. This study demonstrated that palmitate availability affected β cell AMPK activity. In β cells, an increase in AMPK activity may be required for fatty acid-induced fatty acid oxidation and prevention of lipotoxicity.