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pubmed-article:20980454pubmed:abstractTextThe 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(ATP)-induced HI in two probands and to characterize the clinical course.lld:pubmed
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pubmed-article:20980454pubmed:articleTitleCongenital hyperinsulinism and glucose hypersensitivity in homozygous and heterozygous carriers of Kir6.2 (KCNJ11) mutation V290M mutation: K(ATP) channel inactivation mechanism and clinical management.lld:pubmed
pubmed-article:20980454pubmed:affiliationDepartment of Pediatrics, University of North Carolina School of Medicine, Chapel Hill, USA.lld:pubmed
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