Type 2 Diabetes-a Matter of ß-Cell Life and Death?

By C. Rhodes. Science, 2005

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The role for endoplasmic reticulum stress in diabetes mellitus. (2008, background): “Insulin mRNA is translational quiescent at low (Ͻ3 mm) glucose concentrations, but after stimulation by higher glucose concentrations there is a greater than 10-fold increase in biosynthesis (172–174).”
Endoplasmic reticulum stress contributes to beta cell apoptosis in type 2 diabetes (2007, background): “Time-course changes in apoptosis in MIN6 cells exposed to elevated lipids As with primary beta cells, chronic exposure of the MIN6 cell line [21] to elevated fatty acids leads to secretory defects and enhanced apoptosis, which are reminiscent of the beta cell phenotype displayed in type 2 diabetes [”
Mechanisms linking obesity to insulin resistance and type 2 diabetes (2006, background): “Activation of the insulin/IGF-1 receptor leads to phosphorylation of IRS-2 and downstream signalling through pathways including PI(3)K/protein kinase-B (PKB/Akt) and Ras, leading to activation of the mitogen-activated protein (MAP) kinases ERK-1 and ERK-2 (ref”
Autophagy is important in islet homeostasis and compensatory increase of beta cell mass in response to high-fat diet. (2008, neutral): “Recent studies have shown that progressively decreased pancreatic b cell function and b cell mass are common features of subjects with type 2 diabetes mellitus (Butler et al., 2003; Rhodes, 2005).”