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slc30A8 colocalizes with ghrelin and motilin in the gastrointestinal tract of pigs
The absence of ZnT8 in glucagon-producing cells in pig islets indicates that zinc homeostasis is mediated by a different cellular mechanism compared with human islet cells.
Knockin mouse model suggests that the SLC30A8 R138X loss-of-function mutation may exert beneficial effects on glucose metabolism by increasing the capacity of beta-cells to secrete insulin under hyperglycemic conditions.
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.
Our findings demonstrate that glucose homeostasis in the mouse improves as beta-cell ZnT8 activity increases, and remarkably, these changes track Zn(2+) rather than insulin release in vitro.
Deletion of ZnT8 in a limited subset ( approximately 15%) of alpha-pancreatic cells is sufficient to increase glucagon secretion at low glucose concentrations in vitro and in vivo and to improve the response to hypoglycemia.
ischemic retinopathy maybe mediated by aberrant Zn(++) homeostasis caused by ZnT8 downregulation, whereas YC-1 plays a neuroprotective role against ischemic insult
Data suggest that, despite a marked reduction in islet zinc content, the absence of ZnT-8 does not have a substantial impact on mouse physiology.
Beta-cell Znt8 alone does not considerably aggravate weight gain and glucose intolerance during metabolic stress imposed by an high-fat high-calorie diet. Global loss of Znt8 is involved in diet-induced obesity and resulting insulin resistance.
Downregulation of ZnT8 may be associated with impaired function of beta-cells in diabetes.
Mutation of two Pdx-1-binding sites in enhancer A markedly reduces fusion gene expression suggesting that this factor contributes to Slc30a8 expression in beta-c
Our data indicate that while, under the conditions studied, ZnT8 is absolutely essential for proper beta cell function, it is largely dispensable for alpha cell function.
Results suggest that an acute decrease in ZnT8 levels impairs beta-cell function and Zn homeostasis, and may contribute to inflammatory cytokine-induced alterations in beta-cell function.
Diabetes-linked zinc transporter ZnT8 is a homodimeric protein expressed by distinct rodent endocrine cell types in the pancreas and other glands.
Slc30a8 gene deletion is accompanied by a modest impairment in insulin secretion without major alterations in glucose metabolism.
ZnT8 is required for normal insulin crystallization and insulin release in vivo but not, remarkably, in vitro
ZnT8 transporter is essential for the formation of insulin crystals in beta cells, contributing to the packaging efficiency of stored insulin.
Polymorphisms in SLC30A8 is associated with Polycystic ovary syndrome and type-2 diabetes.
The prevalence of Zinc transporter 8 antibody in Thai juvenile-onset type 1 diabetes mellitus appears to be higher than in previous studies from Asia.
ZnT8 Arg325Trp polymorphism is associated with enhanced inflammation in type 2 diabetes.
the effects of the interaction between ZNT8 rs13266634 and dietary factors on the risk of Metabolic syndrome S were investigated in this study.
HLA-A*24, the SLC30A8 T allele and high BMI are associated with poor graft outcome in type 1 diabetics undergoing pancreatic islet transplantation.
The findings reported herein that the diabetes risk genotype C/C at SNP rs13266634 of the SLC30A8 gene encoding the beta-cell Zn transporter ZnT8 is associated with a higher total islet Zn concentration, is potentially of clinical significance.
Results demonstrate that SLC30A8 rs2466293 was associated with T1D predisposition in brazilians with non-European descents.
is a valuable biological marker to classify newly-diagnosed diabetics
common single nucleotide polymorphisms confer risk susceptibility to type 2 diabetes; DNA methylation levels are increased in type 2 diabetes patients [review]
These findings of differential cytolocation of ZnT8 isoforms could be relevant for beta-cell zinc metabolism in health and disease.
rs13266634/T SNP (SLC30A8) is a suggestive protective variant against gestational diabetes mellitus development.
High Arg-325 variant in ZnT8 is associated with Risk for Type-2 Diabetes.
The results provide a strong evidence for independent association between type 2 diabetes mellitus and SNPs for in TCF7L2 and SLC30A8.
this is the first study to report a significant association between the R325W C-allele of SLC30A8 and increased risk of developing gestational diabetes mellitus. All of the autoantibody positive women with GDM who developed postpartum type 1 diabetes were positive for autoantibodies against glutamic acid decarboxylase. Thus ZnT8A did not have any additional predictive value in postpartum development of type 1 diabetes.
Although previous meta-analyses have shown that this association was only found in Asian and European groups, and not in African populations, our analysis revealed the deleterious effect of SLC30A8 rs13266634 on type 2 diabetes mellitus in an African population when stratified by ethnicity under additive model even with a small number of studies.
Results indicate a lack of association of the SLC30A8 SNPs with type 2 diabetes in Mexican American families.
The hZnT8 R325W transgenic line had lower pancreatic [Zn(2+)]i and proinsulin and higher insulin and glucose tolerance compared with control littermates after 10 weeks of a high-fat diet in male mice. The converse was true for the hZnT8 WT transgenic line, and dietary Zn(2+) supplementation also induced glucose intolerance.
Data indicate that gestational weight gain may modify SLC30A8 variant on long-term glycemic changes, highlighting the importance of gestational weight control in the prevention of postpartum hyperglycemia in women with GDM.
We investigated the association of the polymorphisms rs13266634 (SLC30A8) in a case-control study in Euro-Brazilians with gestational diabetes. The minor allele frequencies, for healthy and gestational diabetes, respectively, for the T-allele (SLC30A8 gene rs13266634) were 27.8% (95%CI = 23-32%) vs 23.5% (95%CI = 18-29%), P = 0.227. Genotype comparisons showed no significant difference.
Two miR-binding SNPs SLC30A8 rs2466293 and INSR rs1366600 increased Gestational diabetes mellitus susceptibility. Functional studies were required to confirm the underlying mechanism.
The protein encoded by this gene is a zinc efflux transporter involved in the accumulation of zinc in intracellular vesicles. This gene is expressed at a high level only in the pancreas, particularly in islets of Langerhans. The encoded protein colocalizes with insulin in the secretory pathway granules of the insulin-secreting INS-1 cells. Allelic variants of this gene exist that confer susceptibility to diabetes mellitus, noninsulin-dependent (NIDDM). Several transcript variants encoding different isoforms have been found for this gene.
solute carrier family 30 (zinc transporter), member 8
, zinc transporter 8-like
, solute carrier family 30 member 8
, zinc transporter 8
, solute carrier family 30 (zinc transporter), member 3
, zinc transporter ZnT-8
, LOW QUALITY PROTEIN: uncharacterized protein slc30a8