Journal
ENDOCRINOLOGY
Volume 150, Issue 3, Pages 1132-1139Publisher
ENDOCRINE SOC
DOI: 10.1210/en.2008-0991
Keywords
-
Categories
Funding
- National Institutes of Health [NS29709]
- National Science Foundation [DGE-0440525]
- National Institute of General Medical Sciences [T32 GM08307]
Ask authors/readers for more resources
Glucose-stimulated insulin and glucagon release regulates glucose homeostasis by an excitation-secretion coupling pathway beginning with ATP-sensitive K+ channel closure, membrane depolarization, and entry of calcium ions to stimulate exocytosis. The contribution of voltage-gated sodium channels to this release pathway is still being elucidated. We demonstrate that loss of Scn1b, a major regulatory subunit expressed with Na(v)1.7 protein in mouse pancreatic islets, reduces glucose-stimulated insulin and glucagon secretion in vitro and in vivo, resulting in severe fed and fasting hypoglycemia. This genetic mouse model is the first to demonstrate that sodium channelopathy impairs the physiological excitation-release coupling pathway for pancreatic insulin and glucagon release. (Endocrinology 150: 1132-1139, 2009)
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