ArticleMolecular endocrinology (Baltimore, Md.)2016
Molecular Genetic Regulation of Slc30a8/ZnT8 Reveals a Positive Association With Glucose Tolerance.
Article in Molecular endocrinology (Baltimore, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Expression of the ZIP/SLC39A transporters in β-cells: a systematic review and integration of multiple datasets.BMC genomics · 2017Pooled it
- Zinc Homeostasis and the Risk of Type 2 Diabetes: Complex Role of ZnT8 in Insulin and Glucagon Secretion.Current nutrition reports · 2026Review
- Correlative imaging reveals metal dyshomeostasis and altered zinc coordination environments in a pre-clinical Type 2 diabetes model.Metallomics : integrated biometal science · 2026Article
- High Serum Zinc Concentration Accelerates Progression of Isolated Impaired Glucose Tolerance to Type 2 Diabetes: A Cohort Study.Biological trace element research · 2025Article
- Characterizing the effects of Dechlorane Plus on β-cells: a comparative study across models and species.Islets · 2024Article
- Exploring pancreatic beta-cell subgroups and their connectivity.Nature metabolism · 2024Review
- Metabolic basis of solute carrier transporters in treatment of type 2 diabetes mellitus.Acta pharmaceutica Sinica. B · 2024Review
- Relationship Between the Single Nucleotide Polymorphism rs11558471 in the SLC30A8/ZnT8 Gene and Cardiometabolic Markers in Postmenopausal Women.Biological trace element research · 2023Article
- Article
- Imaging zinc trafficking in vivo by positron emission tomography with zinc-62.Metallomics : integrated biometal science · 2022Article
- Article
- Non-invasive radionuclide imaging of trace metal trafficking in health and disease: "PET metallomics".RSC chemical biology · 2022Review
- The Oxidative Balance Orchestrates the Main Keystones of the Functional Activity of Cardiomyocytes.Oxidative medicine and cellular longevity · 2022Review
- Zinc transporter 8 (ZnT8) autoantibody prevalence in black South African participants with type 1 diabetes.BMC endocrine disorders · 2021Article
- Loss of Znt8 function in diabetes mellitus: risk or benefit?Molecular and cellular biochemistry · 2021Review
- Pancreatic β cell-selective zinc transporter 8 insufficiency accelerates diabetes associated with islet amyloidosis.JCI insight · 2021Article
- Article
- Restoration of mRNA Expression of Solute Carrier Proteins in Liver of Diet-Induced Obese Mice by Metformin.Frontiers in endocrinology · 2021Article
- SNPs in the 3'-untranslated region ofJournal of diabetes and metabolic disorders · 2020Article
- The type 2 diabetes gene product STARD10 is a phosphoinositide-binding protein that controls insulin secretory granule biogenesis.Molecular metabolism · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Zinc transporter 8 (ZnT8), encoded by SLC30A8, is chiefly expressed within pancreatic islet cells, where it mediates zinc (Zn(2+)) uptake into secretory granules. Although a common nonsynonymous polymorphism (R325W), which lowers activity, is associated with increased type 2 diabetes (T2D) risk, rare inactivating mutations in SLC30A8 have been reported to protect against T2D. Here, we generate and characterize new mouse models to explore the impact on glucose homeostasis of graded changes in ZnT8 activity in the β-cell. Firstly, Slc30a8 was deleted highly selectively in these cells using the novel deleter strain, Ins1Cre. The resultant Ins1CreZnT8KO mice displayed significant (P < .05) impairments in glucose tolerance at 10 weeks of age vs littermate controls, and glucose-induced increases in circulating insulin were inhibited in vivo. Although insulin release from Ins1CreZnT8KO islets was normal, Zn(2+) release was severely impaired. Conversely, transgenic ZnT8Tg mice, overexpressing the transporter inducibly in the adult β-cell using an insulin promoter-dependent Tet-On system, showed significant (P < .01) improvements in glucose tolerance compared with control animals. Glucose-induced insulin secretion from ZnT8Tg islets was severely impaired, whereas Zn(2+) release was significantly enhanced. Our findings demonstrate that glucose homeostasis in the mouse improves as β-cell ZnT8 activity increases, and remarkably, these changes track Zn(2+) rather than insulin release in vitro. Activation of ZnT8 in β-cells might therefore provide the basis of a novel approach to treating T2D.
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