Insulin protects islets from apoptosis via Pdx1 and specific changes in the human islet proteome.

ABSTRACT: Insulin is both a hormone regulating energy metabolism and a growth factor. We and others have shown that physiological doses of insulin initiate complex signals in primary human and mouse beta-cells, but the functional significance of insulin's effects on this cell type remains unclear. In the present study, the role of insulin in beta-cell apoptosis was examined. Exogenous insulin completely prevented apoptosis induced by serum withdrawal when given at picomolar or low nanomolar concentrations but not at higher concentrations, indicating that physiological concentrations of insulin are antiapoptotic and that insulin signaling is self-limiting in islets. Insulin treatment was associated with the nuclear localization of Pdx1 and the prosurvival effects of insulin were largely absent in isl

SUBMITTER: Johnson JD 

PROVIDER: S-EPMC1748267 | biostudies-literature | 2006 Dec

REPOSITORIES: biostudies-literature