Journal
DIABETES
Volume 54, Issue 1, Pages 125-132Publisher
AMER DIABETES ASSOC
DOI: 10.2337/diabetes.54.1.125
Keywords
-
Categories
Ask authors/readers for more resources
Glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells depends on coordinated glucose uptake, oxidative metabolism, and Ca2+-triggered insulin exocytosis. Impaired GSIS is a hallmark of type 2 diabetes. However, at present we know very little about the molecular mechanisms that induce and maintain the expression of genes required for GSIS in beta-cells. The transcription factor nuclear factor-kappaB (NF-kappaB) is activated by an increase in intracellular Ca2+ in beta-cells. Here, we show that attenuation of NF-kappaB activation in beta-cells generates mice with impaired GSIS, and that the beta-cells show perturbed expression of genes required for glucose uptake, oxidative metabolism, and insulin exocytosis. Thus, NF-kappaB appears to be part of a positive regulatory circuit that maintains GSIS in pancreatic beta-cells.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available