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Measuring Relative Insulin Secretion using a Co-Secreted Luciferase Surrogate

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Zinc, alpha cells and glucagon secretion.

Laerke Egefjord¹, Andreas B Petersen, Jørgen Rungby

¹Department of Pharmacology, University of Aarhus, Aarhus, Denmark. le@studmed.au.dk

Current Diabetes Reviews

|December 26, 2009

Summary

Zinc plays a key role in regulating glucagon secretion from alpha-cells and maintaining islet cell function. Its transporters, like ZnT8, are linked to diabetes risk, impacting both alpha- and beta-cell functions.

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Area of Science:

Endocrinology
Cell Biology
Metabolic Research

Background:

Zinc is concentrated in islet cells and influences insulin secretion.
Paracrine and autocrine regulation significantly impact islet hormone secretion.
Zinc acts as a potential paracrine inhibitor of glucagon secretion in alpha-cells.

Purpose of the Study:

To review recent data on zinc's role in alpha-cell function.
To highlight the significance of zinc transporters, particularly ZnT8, in diabetes.
To discuss the impact of zinc homeostasis on islet cell mass and survival.

Main Methods:

Localization of free zinc ions and zinc transporters (SLC39A and SLC30A families) in alpha-cells.
Investigation of the role of redox state and Voltage Gated Calcium Channels (VGCC) in zinc homeostasis.
Analysis of genetic data linking ZnT8 to type 1 and type 2 diabetes.

Main Results:

Zinc transporters ZIP1, ZIP10, ZIP14, ZnT1, and ZnT4-8 are present in alpha-cells.
ZnT8 is identified as a genetic risk factor for type 1 and type 2 diabetes.
Emerging data suggest specific effects of Zn2+ on glucagon secretion and alpha-cell function.

Conclusions:

Zinc homeostasis is critical for alpha-cell function and survival.
Dysregulation of zinc transport, especially via ZnT8, is implicated in diabetes.
Further research into zinc's role in alpha-cells is warranted for understanding and treating diabetes.