Congenital Hyperinsulinism and Glucose Hypersensitivity in Homozygous and Heterozygous Carriers of Kir6.2 (KCNJ11) Mutation V290M Mutation: K(ATP) Channel Inactivation Mechanism and Clinical Management

OBJECTIVE: The ATP-sensitive K(+) channel (K(ATP)) controls insulin secretion from the islet. Gain- or loss-of-function mutations in channel subunits underlie human neonatal diabetes and congenital hyperinsulinism (HI), respectively. In this study, we sought to identify the mechanistic basis of K(AT...

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Bibliographic Details
Main Authors: Loechner, Karen J., Akrouh, Alejandro, Kurata, Harley T., Dionisi-Vici, Carlo, Maiorana, Arianna, Pizzoferro, Milena, Rufini, Vittoria, de Ville de Goyet, Jean, Colombo, Carlo, Barbetti, Fabrizio, Koster, Joseph C., Nichols, Colin G.
Format: Artigo
Language:Inglês
Published: American Diabetes Association 2011
Subjects:
Islet Studies
Online Access:https://ncbi.nlm.nih.gov/pmc/articles/PMC3012173/
https://ncbi.nlm.nih.gov/pubmed/20980454
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.2337/db10-0731
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