Chronic Effects of Palmitate Overload on Nutrient-Induced Insulin Secretion and Autocrine Signalling in Pancreatic MIN6 Beta Cells

Abstract

Our results exclude changes in ceramide content or mitochondrial fatty acid handling as factors initiating palmitate-induced defects in insulin release from MIN6 β cells, but suggest that reduced CaMKII and ERK activation associated with palmitate overload may contribute to impaired stimulus-induced insulin secretion.