Here are the Beta cell specific ZnT8 gene deficiency and resulting loss in zinc content significantly improve insulin secretion journals presenting the latest research across various disciplines. From social sciences to technology, each article is expected to provide valuable insights to our readers.
What are beta cells, specific location of beta cell, cd8 positive alpha beta t cell, znt8 antibodies type 1 diabetes, beta cell supplements, what is znt8 antibodies, cell phone beta testing.
Beta cell specific ZnT8 gene deficiency and resulting loss in zinc content significantly improve insulin secretion
Zinc transporter 8 (ZnT8) is highly expressed in pancreatic beta cells, localizes to insulin secretory granules (ISG), and regulates zinc content. ZnT8 gene polymorphisms have revealed a relationship between ZnT8 activity and type 2 diabetes (T2D) risk, however, the role of beta-cell ZnT8 is not well understood. A beta cell specific ZnT8 knockout (ZnT8 BKO) mouse model was investigated. ZnT8 BKO islets showed significantly reduced ZnT8 gene expression and reduced zinc content. Compared to controls, ZnT8 BKO mice displayed significantly elevated plasma insulin levels and improved glucose tolerance following acute insulin resistance induced via S961. Glucose stimulated insulin secretion from isolated ZnT8 BKO pancreatic islets revealed enhanced insulin secretion capacity. The difference in insulin secretion between ZnT8 BKO and control islets was negated upon zinc supplementation, and the inhibitory effect of zinc on insulin secretion was confirmed in human islets. These result s indicate that the loss of ZnT8 activity and accompanying reduced cellular zinc are associated with increased insulin secretion capacity. The reduction in secreted insulin content upon zinc supplementation in ZnT8 BKO islets suggests that ISG-released zinc normally tempers insulin secretion. © 2024 The Authors
Authors : Piro A.; Luo Y.; Zhang Z.; Ye W.; Kang F.; Xie L.; Wang Y.; Dai F.F.; Gaisano H.Y.; Rocheleau J.V.; Prentice K.J.; Wheeler M.B.
Source : Elsevier Ireland Ltd
Article Information
| Year | 2024 |
| Type | Article |
| DOI | 10.1016/j.mce.2024.112376 |
| ISSN | 03037207 |
| Volume | 594 |
You can download the article here
If You have any problem, contact us here