Giatgen A. Spinas

TL;DR: In vitro exposure of islets from nondiabetic organ donors to high glucose levels resulted in increased production and release of IL-1beta, followed by NF-kappaB activation, Fas upregulation, DNA fragmentation, and impaired beta cell function, which implicate an inflammatory process in the pathogenesis of glucotoxicity in type 2 diabetes.

TL;DR: The results suggest that the lipotoxic effect of the saturated palmitic acid involves an increased apoptosis rate coupled with reduced proliferation capacity of beta-cells and impaired insulin secretion, and the monounsaturated palmitoleic acid promotes beta-cell proliferation at low glucose concentrations, counteracting the negative effects of palmitoic acid as well as improving beta- cell function.

TL;DR: In human islets, the saturated palmitic acid and elevated glucose concentration induce beta-cell apoptosis, decreasebeta-cell proliferation, and impair beta- cell function, which can be prevented by monounsaturated fatty acids.

TL;DR: An Internet-based, interactive computer model to determine the longterm health outcomes and economic consequences of implementing different treatment policies or interventions in type 1 and type 2 diabetes mellitus, based on the best data currently available.

TL;DR: A new role for glucose in regulating Fas expression in human beta-cells is supported and may contribute to beta-cell destruction by the constitutively expressed FasL independent of an autoimmune reaction, thus providing a link between type 1 and type 2 diabetes.