کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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4169238 | 1607560 | 2006 | 6 صفحه PDF | دانلود رایگان |
ObjectiveBecause children with congenital hyperinsulinism (HI) caused by recessive loss of function mutations in the adenosine triphosphate (ATP)-dependent potassium channel (KATP-HI) are not leucine sensitive, we evaluated for protein-induced hypoglycemia with oral protein tolerance tests.Study designBlood glucose and insulin concentrations were measured every 15 minutes for 3 hours after an oral protein load in children with KATP-HI (n = 11) and compared with those of children with glutamate dehydrogenase HI (n = 12) and control subjects (n = 12).ResultsSimilar to children with glutamate dehydrogenase HI, patients with KATP-HI displayed protein-induced hypoglycemia (10/11) with blood glucose concentrations declining by 17 to 69 mg/dL. In contrast, oral protein had little effect on blood glucose concentrations in control subjects.ConclusionsProtein-induced hypoglycemia is a feature of KATP-HI, despite the absence of leucine sensitivity. The results indicate that amino acids can stimulate insulin secretion via a glutamate dehydrogenase- and KATP channel-independent pathway.
Journal: The Journal of Pediatrics - Volume 149, Issue 1, July 2006, Pages 47–52