ArticleEndocrinology2016
Combined Deletion of Slc30a7 and Slc30a8 Unmasks a Critical Role for ZnT8 in Glucose-Stimulated Insulin Secretion.
Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Zinc Homeostasis and the Risk of Type 2 Diabetes: Complex Role of ZnT8 in Insulin and Glucagon Secretion.Current nutrition reports · 2026Review
- Loss-of-function variant of SLC30A8 rs13266634 (C > T) protects against type 2 diabetes by stabilizing ZnT8: Insights from epidemiological and computational analyses.Journal, genetic engineering & biotechnology · 2025Article
- Complete loss of SLC30A8 in humans improves glucose metabolism and beta cell function.Diabetologia · 2025Article
- SLC30 (ZnT) and SLC39 (ZIP) zinc transporter families: from gatekeepers of zinc homeostasis to promoters of tumorigenesis and targets for clinical therapy.Frontiers in immunology · 2025Review
- Lack of ZnT8 protects pancreatic islets from hypoxia- and cytokine-induced cell death.The Journal of endocrinology · 2022Article
- Inside the Insulin Secretory Granule.Metabolites · 2021Review
- Loss of Znt8 function in diabetes mellitus: risk or benefit?Molecular and cellular biochemistry · 2021Review
- Insulin granule biogenesis and exocytosis.Cellular and molecular life sciences : CMLS · 2021Review
- Zinc.Advances in food and nutrition research · 2021Review
- SNPs in the 3'-untranslated region ofJournal of diabetes and metabolic disorders · 2020Article
- Potential positive and negative consequences of ZnT8 inhibition.The Journal of endocrinology · 2020Article
- Pancreatic islet beta cell-specific deletion of G6pc2 reduces fasting blood glucose.Journal of molecular endocrinology · 2020Article
- Zinc deficiency alters the susceptibility of pancreatic beta cells (INS-1) to arsenic exposure.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2019Article
- Zinc and its regulators in pancreas.Inflammopharmacology · 2019Review
- Predicting human disease mutations and identifying drug targets from mouse gene knockout phenotyping campaigns.Disease models & mechanisms · 2019Review
- Genetic, Functional, and Immunological Study of ZnT8 in Diabetes.International journal of endocrinology · 2019Review
- The SLC transporter in nutrient and metabolic sensing, regulation, and drug development.Journal of molecular cell biology · 2019Article
- The Diabetes Susceptibility Gene SLC30A8 that Encodes the Zinc Transporter ZnT8 is a Pseudogene in Guinea Pigs Potentially Contributing to Low Guinea Pig Islet Zinc Content.Journal of molecular evolution · 2018Article
- Regulation of islet glucagon secretion: Beyond calcium.Diabetes, obesity & metabolism · 2018Review
- Cooperative function of Pdx1 and Oc1 in multipotent pancreatic progenitors impacts postnatal islet maturation and adaptability.American journal of physiology. Endocrinology and metabolism · 2018Article
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10 authors at 3 institutions in 1 country.
Funding
Abstract
Polymorphisms in the SLC30A8 gene, which encodes the ZnT8 zinc transporter, are associated with altered susceptibility to type 2 diabetes (T2D), and SLC30A8 haploinsufficiency is protective against the development of T2D in obese humans. SLC30A8 is predominantly expressed in pancreatic islet β-cells, but surprisingly, multiple knockout mouse studies have shown little effect of Slc30a8 deletion on glucose tolerance or glucose-stimulated insulin secretion (GSIS). Multiple other Slc30a isoforms are expressed at low levels in pancreatic islets. We hypothesized that functional compensation by the Slc30a7 isoform, which encodes ZnT7, limits the impact of Slc30a8 deletion on islet function. We therefore analyzed the effect of Slc30a7 deletion alone or in combination with Slc30a8 on in vivo glucose metabolism and GSIS in isolated islets. Deletion of Slc30a7 alone had complex effects in vivo, impairing glucose tolerance and reducing the glucose-stimulated increase in plasma insulin levels, hepatic glycogen levels, and pancreatic insulin content. Slc30a7 deletion also affected islet morphology and increased the ratio of islet α- to β-cells. However, deletion of Slc30a7 alone had no effect on GSIS in isolated islets, whereas combined deletion of Slc30a7 and Slc30a8 abolished GSIS. These data demonstrate that the function of ZnT8 in islets can be unmasked by removal of ZnT7 and imply that ZnT8 may affect T2D susceptibility through actions in other tissues where it is expressed at low levels rather than through effects on pancreatic islet function.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.