Cholinergic augmentation of insulin release requires ankyrin-B.

Healy, J.A., Nilsson, K.R., Hohmeier, H.E., Berglund, J., Davis, J., Hoffman, J., Kohler, M., Li, .LS., Berggren, P.O., Newgard, C.B., Bennett, V.
Journal   Sci Signal.
Species  
Analytes Measured   GLP-1
Matrix Tested   Serum
Year   2010
Volume   3
Page Numbers   ra19
Application   Metabolic
Abstract
Parasympathetic stimulation of pancreatic islets augments glucose-stimulated insulin secretion by inducing inositol trisphosphate receptor (IP(3)R)-mediated calcium ion (Ca2+) release. Ankyrin-B binds to the IP(3)R and is enriched in pancreatic beta cells. We found that ankyrin-B-deficient islets displayed impaired potentiation of insulin secretion by the muscarinic agonist carbachol, blunted carbachol-mediated intracellular Ca2+ release, and reduced the abundance of IP3R. Ankyrin-B-haploinsufficient mice exhibited hyperglycemia after oral ingestion but not after intraperitoneal injection of glucose, consistent with impaired parasympathetic potentiation of glucose-stimulated insulin secretion. The R1788W mutation of ankyrin-B impaired its function in pancreatic islets and is associated with type 2 diabetes in Caucasians and Hispanics. Thus, defective glycemic regulation through loss of ankyrin-B-dependent stabilization of IP3R is a potential risk factor for type 2 diabetes.

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