Beta cell-specific Znt8 deletion in mice causes marked defects in insulin processing, crystallisation and secretion.

ABSTRACT:

Aims/hypothesis

Zinc is highly concentrated in pancreatic beta cells, is critical for normal insulin storage and may regulate glucagon secretion from alpha cells. Zinc transport family member 8 (ZnT8) is a zinc efflux transporter that is highly abundant in beta cells. Polymorphisms of ZnT8 (also known as SLC30A8) gene in man are associated with increased risk of type 2 diabetes. While global Znt8 knockout (Znt8KO) mice have been characterised, ZnT8 is also present in other islet cell types and extra-pancreatic tissues. Therefore, it is important to find ways of understanding the role of ZnT8 in beta and alpha cells without the difficulties caused by the confounding effects of ZnT8 in these other tissues.

Methods

We generated mice with beta cell-specific (Znt8BKO) and alpha c

SUBMITTER: Wijesekara N 

PROVIDER: S-EPMC6101216 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature