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...

Descripción completa

Detalles Bibliográficos
Autores principales: 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.
Formato: Texto
Lenguaje:English
Publicado: American Diabetes Association 2011
Materias:
Islet Studies
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3012173/
https://www.ncbi.nlm.nih.gov/pubmed/20980454
http://dx.doi.org/10.2337/db10-0731

Ejemplares similares

Ejemplares similares