Phenotype of a transient neonatal diabetes point mutation (SUR1-R1183W) in mice.

ABSTRACT: Background: The K _ATP channel plays a key role in glucose homeostasis by coupling metabolically generated changes in ATP to insulin secretion from pancreatic beta-cells.  Gain-of-function mutations in either the pore-forming (Kir6.2) or regulatory (SUR1) subunit of this channel are a common cause of transient neonatal diabetes mellitus (TNDM), in which diabetes presents shortly after birth but remits within the first few years of life, only to return in later life. The reasons behind this time dependence are unclear. Methods: In an attempt to understand the mechanism behind diabetes remission and relapse, we generated mice expressing the common TNDM mutation SUR1-R1183W. We employed Cre/LoxP technology for both inducible and constitutive expression of SUR1-R1183W s

SUBMITTER: Sachse G 

PROVIDER: S-EPMC8323074 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature