Generic placeholder image

Current Diabetes Reviews

Editor-in-Chief

ISSN (Print): 1573-3998
ISSN (Online): 1875-6417

Zinc, Alpha Cells and Glucagon Secretion

Author(s): Laerke Egefjord, Andreas B. Petersen, Ann M. Bak and Jorgen Rungby

Volume 6, Issue 1, 2010

Page: [52 - 57] Pages: 6

DOI: 10.2174/157339910790442655

Price: $65

Abstract

Zinc concentrates in islet cells and is related to insulin secretion. Islet cells act as a unit within islets and hormone secretion in the islets is profoundly influenced by paracrine and autocrine regulation. Zinc has been recognised as a candidate paracrine inhibitor of glucagon secretion in α-cells. Further zinc fluxes may contribute to regulation of cell mass, Zn2+ may be cytotoxic and Zn2+ depletion by itself can cause cell death induced by oxidative stress. Recently, both free zinc ions and a number of zinc transporters have been localized in α-cells. These include zinc importers, ZIP1, ZIP10, and ZIP14 of the SLC39A family and zinc exporters, ZnT1, and ZnT4-8 of the SLC30A family. Furthermore, the redox state of thiol groups and Voltage Gated Ca2+ Channels (VGCC) add to the maintenance of a tight cytoplasmatic zinc homeostasis in the α-cells. The ZnT8 protein has emerged as particularly interesting since this zinc transporter has been identified as a genetic risk factor for the development of both type 1 and type 2 diabetes in which both α- and β-cell functions are affected. Recent data discussed here suggest specific effects of Zn2+ on glucagon secretion and other α-cell functions.

Keywords: Pancreas, Diabetes, α-cells, Glucagon, Zinc transporters, Zn2+


Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy