Ask about this productRelated genes to: SLC30A8 Blocking Peptide
- Gene:
- SLC30A8 NIH gene
- Name:
- solute carrier family 30 member 8
- Previous symbol:
- -
- Synonyms:
- ZnT-8, ZNT8
- Chromosome:
- 8q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-14
- Date modifiied:
- 2016-12-13
Related products to: SLC30A8 Blocking Peptide
Related articles to: SLC30A8 Blocking Peptide
- (1) Loss-of-function mutations in , encoding the zinc ion (Zn ) transporter ZnT8 in pancreatic beta cells, lower type 2 diabetes risk dose-dependently, but the underlying mechanisms remain unclear. Here, we combine proteomic, transcriptomic and functional approaches in human stem cell-derived islet-like clusters bearing common alleles or the inactivating variant R138X. We hypothesized that this variant protects against the deleterious effect of Zn depletion on cell survival and function. - Source: PubMed
Publication date: 2026/04/20
Gasser MarieCherkaoui InèsOstinelli GiadaFerron MathieuDu QianEgli DieterRutter Guy A - - Source: PubMed
Publication date: 2026/04/25
Ghafouri-Taleghani FatemeBahadoran Zahra - Type 2 diabetes (T2DM) is a metabolic disease characterized by chronic hyperglycemia. We investigated the relationship between the polymorphisms of KCNJ11, of TCF7L2, and of SLC30A8 in a Gabonese population with T2DM. - Source: PubMed
Publication date: 2026/02/15
Mbang Bengone Aude SNikiema-Ndong RosalieBatou Alvine SNnegue Edzo EdwigeDa Dari FrédéricOvono Abessolo Felix - The classification of early onset (< 30 years old) patients with diabetes mellitus (DM) as either type 1 diabetes (T1D) or type 2 diabetes (T2D) can be a challenge due to their similar overlapping phenotypes. In this study, we attempted to utilize various clinical and laboratory characteristics in combination with immunological factors in the blood to determine whether it would be possible to distinguish and more accurately characterize our patients as T2D. - Source: PubMed
Publication date: 2026/02/23
Lee Dong-HwaJeon Hyun JeongOh Tae Keun - Gestational diabetes mellitus (GDM) is a common metabolic complication of pregnancy associated with significant short- and long-term risks for both mother and offspring. Increasing evidence indicates that genetic susceptibility plays a central role in GDM pathogenesis, particularly through variants affecting insulin secretion and pancreatic β-cell function. This narrative review integrates molecular, clinical, and epidemiological perspectives, highlighting population-specific effects and gene-environment interactions. Improved understanding of the genetic risk architecture may support earlier risk stratification and enable the future development of personalized strategies for GDM prevention and management, with particular emphasis on genetic polymorphisms in , , and genes consistently implicated in glucose homeostasis and β-cell integrity. These genes contribute to distinct but complementary molecular pathways underlying GDM, including impaired insulin biosynthesis, defective zinc transport within insulin granules, and altered paracrine regulation within pancreatic islets. While associations between these variants and GDM have been repeatedly demonstrated, their clinical relevance and mechanistic impact remain incompletely understood. Available evidence suggests that represents the strongest genetic determinant, followed by , while appears to play a modulatory role. This review summarizes current findings on the molecular functions and clinical significance of these polymorphisms, highlighting population-specific effects and gene-environment interactions. Improved understanding of genetic risk architecture may support earlier risk stratification and enable future development of personalized strategies for GDM prevention and management. - Source: PubMed
Publication date: 2026/01/22
Hryniewicka JustynaBuczyńska-Backiel AngelikaZbucka-Krętowska MonikaKrętowski Adam JacekSzelachowska Małgorzata