Genetic, Functional, and Immunological Study of ZnT8 in Diabetes.
Qiong HuangJie DuChengfeng MerrimanZhicheng GongPublished in: International journal of endocrinology (2019)
Zinc level in the body is finely regulated to maintain cellular function. Dysregulation of zinc metabolism may induce a variety of diseases, e.g., diabetes. Zinc participates in insulin synthesis, storage, and secretion by functioning as a "cellular second messenger" in the insulin signaling pathway and glucose homeostasis. The highest zinc concentration is in the pancreas islets. Zinc accumulation in cell granules is manipulated by ZnT8, a zinc transporter expressed predominately in pancreatic α and β cells. A common ZnT8 gene (SLC30A8) polymorphism increases the risk of type 2 diabetes mellitus (T2DM), and rare mutations may present protective effects. In type 1 diabetes mellitus (T1DM), autoantibodies show specificity for binding two variants of ZnT8 (R or W at amino acid 325) dictated by a polymorphism in SLC30A8. In this review, we summarize the structure, feature, functions, and polymorphisms of ZnT8 along with its association with diabetes and explore future study directions.
Keyphrases
- type diabetes
- glycemic control
- oxide nanoparticles
- cardiovascular disease
- signaling pathway
- amino acid
- induced apoptosis
- genome wide
- systemic lupus erythematosus
- machine learning
- single cell
- cell therapy
- cell death
- dna methylation
- transcription factor
- gene expression
- adipose tissue
- mesenchymal stem cells
- oxidative stress
- pi k akt
- cell cycle arrest
- deep learning
- bone marrow
- breast cancer risk