Loss of CtBP2 may be a mechanistic link between metabolic derangements and progressive impairment of pancreatic β cell function

Abstract excerpt

The adaptive increase in insulin secretion in early stages of obesity serves as a safeguard mechanism to maintain glucose homeostasis that cannot be sustained, and the eventual decompensation of β cells is a key event in the pathogenesis of diabetes. Here we describe a crucial system orchestrated by a transcriptional cofactor CtBP2. In cultured β cells, insulin gene expression is coactivated by CtBP2. Global...

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• Genetic Syndromes and Imprinting
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