Abnormal mitochondrial function impairs calcium influx in diabetic mouse pancreatic beta cells.

Fei Li, D Marshall Porterfield, Xi-Yan Zheng, Wen-Jun Wang, Yue Xu, Zong-Ming Zhang

Department of General Surgery, Digestive Medical Center, the First Affiliated Hospital, Medical School, Tsinghua University, Beijing 100016, China.

Chinese medical journal 2012 Feb

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Abnormal insulin secretion of panc reatic beta cells is now regarded as the more primary defect than the insulin function in the etiology of type 2 diabetes. Previous studies found impaired mitochondrial function and impaired Ca(2+) influx in beta cells in diabetic patients and animal models, suggesting a role for these processes in proper insulin secretion. The aim of this study was to investigate the detailed relationship of mitochondrial function, Ca(2+) influx, and defective insulin secretion. We investigated mitochondrial function and morphology in pancreatic beta cell of diabetic KK-Ay mice and C57BL/6J mice. Two types of Ca(2+) channel activities, L-type and store-operated Ca(2+) (SOC), were evaluated using whole-cell patch-clamp recording. The glucose induced Ca(2+) influx was measured by a non-invasive micro-test technique (NMT). Mitochondria in KK-Ay mice pancreatic beta cells were swollen with disordered cristae, and mitochondrial function decreased compared with C57BL/6J mice. Ca(2+) channel activity was increased and glucose induced Ca(2+) influx was impaired, but could be recovered by genipin. Defective mitochondrial function in diabetic mice pancreatic beta cells is a key cause of abnormal insulin secretion by altering Ca(2+) influx, but not via Ca(2+) channel activity.

Citation

Fei Li, D Marshall Porterfield, Xi-Yan Zheng, Wen-Jun Wang, Yue Xu, Zong-Ming Zhang. Abnormal mitochondrial function impairs calcium influx in diabetic mouse pancreatic beta cells. Chinese medical journal. 2012 Feb;125(3):502-10