Endogenous regulation of insulin secretion by UCP2

Abstract

Uncoupling protein 2 (UCP2) expression is more-or-less ubiquitous, in tissues of diverse function. Its presence in adipose and muscle is postulated to be involved in regulation of energy expenditure and nutrient partitioning, particularly that of fats. In pancreatic islet beta cells, induction of UCP2 is shown to inhibit glucose-stimulated insulin secretion. Thus, insufficient insulin secretion in models of type 2 diabetes is associated with elevated UCP2 expression in islets. The evidence for such a role for UCP2 in the regulation of insulin secretion in islets is reviewed.