Int. J. Mol. Sci. 2018, 19(2), 476; https://doi.org/10.3390/ijms19020476
Role of Zinc Homeostasis in the Pathogenesis of Diabetes and Obesity
Laboratory of Developmental Biology & Metabolism, Institute for Molecular & Cellular Regulation, Gunma University, 3-39-15 Showa-machi, Maebashi, Gunma 371-8512, Japan
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Received: 27 November 2017 / Revised: 30 January 2018 / Accepted: 2 February 2018 / Published: 6 February 2018
(This article belongs to the Special Issue Zinc Signaling in Physiology and Pathogenesis)
Abstract
Zinc deficiency is a risk factor for obesity and diabetes. However, until recently, the underlying molecular mechanisms remained unclear. The breakthrough discovery that the common polymorphism in zinc transporter SLC30A8/ZnT8 may increase susceptibility to type 2 diabetes provided novel insights into the role of zinc in diabetes. Our group and others showed that altered ZnT8 function may be involved in the pathogenesis of type 2 diabetes, indicating that the precise control of zinc homeostasis is crucial for maintaining health and preventing various diseases, including lifestyle-associated diseases. Recently, the role of the zinc transporter ZIP13 in the regulation of beige adipocyte biogenesis was clarified, which indicated zinc homeostasis regulation as a possible therapeutic target for obesity and metabolic syndrome. Here we review advances in the role of zinc homeostasis in the pathophysiology of diabetes, and propose that inadequate zinc distribution may affect the onset of diabetes and metabolic diseases by regulating various critical biological events. View Full-TextKeywords:
zinc; zinc transporters; diabetes; obesity; ZnT8; ZIP13; pancreatic β cell; beige adipocyte; therapeutic target
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Fukunaka, A.; Fujitani, Y. Role of Zinc Homeostasis in the Pathogenesis of Diabetes and Obesity. Int. J. Mol. Sci. 2018, 19, 476.
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