Absence of <i>Slc39a14/Zip14</i> in mouse pancreatic beta cells results in hyperinsulinemia-Reference-Cited by-同舟云学术

Absence of Slc39a14/Zip14 in mouse pancreatic beta cells results in hyperinsulinemia

Published:2024-01-01 Issue:1 Volume:326 Page:E92-E105
ISSN:0193-1849
Container-title:American Journal of Physiology-Endocrinology and Metabolism
language:en
Short-container-title:American Journal of Physiology-Endocrinology and Metabolism

Author:

Hung Yu-Han¹²,Kim Yongeun¹,Mitchell Samuel Blake¹,Thorn Trista Lee¹,Aydemir Tolunay Beker¹^ORCID

Affiliation:

1. Division of Nutritional Sciences, Cornell University, Ithaca, New York, United States

2. Department of College of Veterinary Medicine, Cornell University, Ithaca, New York, United States

Abstract

Metal transporter SLC39A14/ZIP14 is downregulated in pancreatic islets of patients with T2D and mouse models of HFD- or db/db-induced obesity. However, the function of ZIP14-mediated intracellular zinc trafficking in β cells is unknown. Our analyses revealed that SLC39A14 is the only Zn transporter expressed abundantly in human β cells besides SLC30A8. Within the β cells, ZIP14 is localized on the endoplasmic reticulum and serves as a negative regulator of insulin secretion, providing a potential therapeutic target for T2D.

Funder

Cornell University

HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology,Endocrinology, Diabetes and Metabolism

Link

https://journals.physiology.org/doi/pdf/10.1152/ajpendo.00117.2023

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