TYPE 2 DIABETES: WHAT IS THE ROLE OF INSULIN IN NF-KAPPAB, PPARϒ AND CD36 EXPRESSION?

Abstract

In both type II diabetes and insulin-resistance syndromes, vascular complications result from a set of atherogenic processes, involving chronic hyperglycemia, excessive protein glycation (AGEs), nuclear factor kappa-B (NF-kappaB) activation associated with inflammatory cytokines superexpression, oxidative stress altering LDL and scavenger receptor CD36 expression. The contribution of hyperinsulinaemia in this sequence is not completely elucidated. This review adresses the modulation of NF-kappaB, PPAR gamma (PPARγ) and CD36 protein expression by insulin in rat aortic vascular smooth muscle cells (VSMCs) stimulated by AGEs.