Publications

Abstract

Isoforms of the protein kinase C family are strong candidates for mediating the inhibitory effects of lipid oversupply on insulin action. These enzymes are lipid-activated, can interfere with insulin signal transduction, and several studies have highlighted an association between insulin resistance and chronic activation of specific protein kinase C isoforms, especially epsilon (var epsilon) and theta (??). The assessment of glucose homeostasis and lipid-induced insulin resistance in protein kinase C ?? knockout mice has now demonstrated a key role for this isoform, although it is not yet clear whether its long-term inhibition would be beneficial. Potential approaches to block the action of specific PKC isoforms include pharmacological inhibitors, antisense oligonucleotides and bioactive peptides.