Phytochemical genistein promotes pancreatic beta-cell survival and exerts anti-diabetic effect via GPR30-mediated mechanism (1045.44)

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