Phytochemical genistein promotes pancreatic beta-cell survival and exerts anti-diabetic effect via GPR30-mediated mechanism (1045.44)
2014
Loss of pancreatic beta-cell mass is central to the development of both type 1 and type 2 diabetes (T2D). Chronic hyperglycemia and hyperlipidemia cause beta-cell apoptosis, thereby contributing to the pathogenesis of T2D. We investigated the effects of phytochemical genistein on apoptosis and function of beta-cells and further determined the mechanism underlying its actions ex vivo and in vivo. We show that genistein promoted viability, inhibited apoptosis, and reduced caspase-3 activity of INS1 beta-cells and human and mouse islets chronically exposed to palmitate (0.5 mM) and high glucose (HG, 20 mM). In addition, exposure of beta-cells to genistein activated PI3K/Akt signaling and up-regulated anti-apoptotic protein Bcl-2 expression. The anti-apoptotic effect of genistein is independent of classical estrogen receptor-mediated signaling machinery, but it may be achieved through the G-protein-coupled receptor GPR30-mediated activation of cAMP signaling. Oral administration of genistein (50 mg/kg BW/day)...
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