Role of Protein Kinase C Isoenzymes in Fatty Acid Stimulation of Insulin Secretion

Although hyperlipidemia is frequently associated with hyperinsulinemia, the stimulation of insulin secretion by fatty acids in the in vitro studies has remained a matter of constant debate, partly because of the uncertainty about a clearly defined mechanism to explain such a direct effect. In this study, we used a pharmacologic approach to test the hypothesis that protein kinase C (PKC) signal-transduction pathway is involved in fatty acid–stimulated insulin secretion. Isolated rat islets were perifused with either palmitate (C160) or linoleate (C182) in the absence or presence of selective inhibitors of PKC isoenzymes. Our results suggest a role for Ca2- independent PKC isoenzymes in the signal transduction of fatty acid–stimulated insulin secretion. The data imply that either the nonconventional and/or atypical isoforms of PKC are involved in the stimulation of insulin release induced by fatty acids.