Abstract
The transition from normal glucose tolerance to impaired glucose tolerance and finally type 2 diabetes mellitus (DM) is driven by the cumulative loss of pancreatic beta-cell function and mass in the background of peripheral insulin resistance. Inflammatory cytokines, e.g. interleukin (IL)-1beta, which are elevated in inflammatory conditions of patients with metabolic diseases, induce beta-cell apoptosis. A protective effect of high density lipoprotein (HDL) on pancreatic beta-cells against high glucose- and IL-1beta-induced apoptosis was described previously. Thus, the goal of this project was to elucidate the mechanism underlying the protective effects of HDL and its components in beta-cells.
Sibler, Rahel