Zinc, a regulator of islet function and glucose homeostasis

被引：113

作者：

Wijesekara, N. ^{[1
]}

Chimienti, F. ^{[2
]}

Wheeler, M. B. ^{[1
,3
]}

机构：

[1] Univ Toronto, Dept Physiol, Toronto, ON M5S 1A8, Canada

[2] Mellitech, Grenoble, France

[3] Univ Toronto, Dept Med, Toronto, ON M5S 1A8, Canada

来源：

DIABETES OBESITY & METABOLISM | 2009年 / 11卷

基金：

加拿大健康研究院;

关键词：

beta-cells; diabetes; insulin secretion; pancreatic islets; SLC30A8; zinc; ZnT8; PANCREATIC BETA-CELLS; TRANSPORTER GENES; RISK LOCI; SLC30A8; GENE; INSULIN; CDKAL1; POLYMORPHISMS; EXPRESSION; CHANNELS; VARIANTS;

D O I：

10.1111/j.1463-1326.2009.01110.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

It is well known that zinc is required in pancreatic beta-cells in the process of insulin biosynthesis and the maturation of insulin secretory granules. In fact, the zinc level in pancreatic islets is amongst the highest in the body and reduction in its levels in the pancreas has been associated with diabetes. High concentrations of zinc can also be toxic because of enhanced oxidative damage. The link between zinc, diabetes and islet dysfunction has recently been reiterated by genomewide association studies that identified an islet cell membrane zinc transporter, SLC30A8 (ZnT8), as one of the risk loci for type 2 diabetes. Here we explore the importance of both zinc and ZnT8 to islet biology and whole body glucose homeostasis.

引用

页码：202 / 214

页数：13

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