Nurit Kaiser

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 capacity of PDX-1 to reprogram extrapancreatic tissue towards a β-cell phenotype, may provide a valuable approach for generating ‘self’ surrogate β cells, suitable for replacing impaired islet-cell function in diabetics.

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: Results suggest that hyperglycemia-induced beta-cell death coupled with reduced proliferative capacity may contribute to the insulin deficiency and deterioration of glucose homeostasis in P. obesus.

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.