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+
Current Diabetes Reviews
Title: Zinc, Alpha Cells and Glucagon Secretion
Volume: 6 Issue: 1
Author(s): Laerke Egefjord, Andreas B. Petersen, Ann M. Bak and Jorgen Rungby
Affiliation:
Keywords: Pancreas, Diabetes, α-cells, Glucagon, Zinc transporters, Zn2+
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.
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Cite this article as:
Egefjord Laerke, Petersen B. Andreas, Bak M. Ann and Rungby Jorgen, Zinc, Alpha Cells and Glucagon Secretion, Current Diabetes Reviews 2010; 6 (1) . https://dx.doi.org/10.2174/157339910790442655
DOI https://dx.doi.org/10.2174/157339910790442655 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |
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