Diabetic hyperglycemia: link to impaired glucose transport in pancreatic beta cells.
Diabetic hyperglycemia: link to impaired glucose transport in pancreatic beta cells.
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DOI：
10.1126/science.2006409
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发表时间：
1991-03
期刊：
影响因子：
56.9
通讯作者：
R. Unger
中科院分区：
文献类型：
--
作者：
R. Unger
葡萄糖转运体GLUT-2具有很高的米氏常数，通过葡萄糖转运体GLUT-2摄取葡萄糖进入胰岛β细胞，对于高血糖时正常的胰岛素分泌反应是必不可少的。在自身免疫性和非自身免疫性糖尿病中，由于正常的β细胞转运蛋白下调，这种葡萄糖转运减少。在自身免疫性糖尿病中，循环免疫球蛋白可以通过抑制功能完整的转运蛋白来进一步损害葡萄糖的运输。深入了解β细胞对高血糖无反应的机制可能会改善糖尿病的管理和预防。
Glucose uptake into pancreatic beta cells by means of the glucose transporter GLUT-2, which has a high Michaelis constant, is essential for the normal insulin secretory response to hyperglycemia. In both autoimmune and nonautoimmune diabetes, this glucose transport is reduced as a consequence of down-regulation of the normal beta-cell transporter. In autoimmune diabetes, circulating immunoglobulins can further impair this glucose transport by inhibiting functionally intact transporters. Insights into mechanisms of the unresponsiveness of beta cells to hyperglycemia may improve the management and prevention of diabetes.