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Zinc transporters and insulin resistance: therapeutic implications for type 2 diabetes and metabolic disease

Norouzi, S ORCID: 0000-0002-7504-8581, Adulcikas, J ORCID: 0000-0001-9193-6709, Sohal, SS ORCID: 0000-0001-9627-6498 and Myers, S ORCID: 0000-0003-4793-3820 2017 , 'Zinc transporters and insulin resistance: therapeutic implications for type 2 diabetes and metabolic disease' , Journal of Biomedical Science, vol. 24 , pp. 1-10 , doi: https://doi.org/10.1186/s12929-017-0394-0.

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Abstract

Background: Zinc is a metal ion that is essential for growth and development, immunity, and metabolism, andtherefore vital for life. Recent studies have highlighted zinc’s dynamic role as an insulin mimetic and a cellular secondmessenger that controls many processes associated with insulin signaling and other downstream pathways that areamendable to glycemic control.Main body: Mechanisms that contribute to the decompartmentalization of zinc and dysfunctional zinc transportermechanisms, including zinc signaling are associated with metabolic disease, including type 2 diabetes. Theactions of the proteins involved in the uptake, storage, compartmentalization and distribution of zinc in cells is underintense investigation. Of these, emerging research has highlighted a role for several zinc transporters in the initiation ofzinc signaling events in cells that lead to metabolic processes associated with maintaining insulin sensitivity and thusglycemic homeostasis.Conclusion: This raises the possibility that zinc transporters could provide novel utility to be targeted experimentallyand in a clinical setting to treat patients with insulin resistance and thus introduce a new class of drug target with utilityfor diabetes pharmacotherapy.

Item Type: Article
Authors/Creators:Norouzi, S and Adulcikas, J and Sohal, SS and Myers, S
Keywords: Zinc transporters, Type 2 diabetes, Insulin resistance
Journal or Publication Title: Journal of Biomedical Science
Publisher: Karger
ISSN: 1021-7770
DOI / ID Number: https://doi.org/10.1186/s12929-017-0394-0
Copyright Information:

© 2017 The Authors. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/

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