DIABETIC HYPERGLYCEMIA - LINK TO IMPAIRED GLUCOSE-TRANSPORT IN PANCREATIC BETA-CELLS

被引：296
|
作者：
UNGER, RH [1 ]
机构：
[1] VET AFFAIRS MED CTR,DALLAS,TX 75235
来源：
SCIENCE | 1991年 / 251卷 / 4998期
关键词：
D O I：
10.1126/science.2006409
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
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.
引用
收藏
页码：1200 / 1205
页数：6
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