Activation of autophagy through modulation of 5′-AMP-activated protein kinase protects pancreatic β-cells from high glucose

摘要: Chronic hyperglycaemia is detrimental to pancreatic beta-cells by causing impaired insulin secretion and diminished beta-cell function through glucotoxicity. Understanding the mechanisms underlying survival crucial for prevention of failure associated with Autophagy a dynamic lysosomal degradation process that protects organisms against metabolic stress. To date, little known about physiological autophagy in pathogenesis diabetes. In present study, we explored roles exposed high glucose using pharmacological genetic manipulation autophagy. We demonstrated chronic increases rat INS-1 (832/13) cells islets, this increase enhanced inhibition 5'-AMP-activated protein kinase. Our results also indicate stimulation rescues from high-glucose-induced cell death augments caspase-3 activation, suggesting plays protective role beta-cells. Greater knowledge molecular linking may unveil novel therapeutic targets needed preserve function.