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• W2461964768 abstract "The study by Vella et al reported in this issue of Endocrine Practice (pages 115-118) had the ambitious goal of establishing reference data for identification of deficiency of glucagon responses to hypoglycemia. In order to do so, the authors took the original and interesting approach of comparing the plasma glucagon concentration at the end of a 72-hour fast in a large group of patients with insulinoma and in normal control subjects. As expected, plasma glucose decreased more in patients with insulinoma in comparison with normal control subjects. Plasma growth hormone and cortisol concentrations increased more in patients with insulinoma, whereas plasma glucagon was lower in patients with insulinoma than in control subjects. In the same study, the authors established that defective counterregulation of glucagon associated with a hypoglycemic disorder is not a generalized phenomenon applicable to other stimuli of glucagon secretion, such as the effect of prolonged withdrawal of food. In fact, in a group of patients with noninsulinoma pancreatogenous hypoglycemia syndrome, who experience postprandial neuroglycopenic hyperinsulinemic hypoglycemia but have normal findings after a 72-hour fast ( 1. Service FJ Natt N. Thompson G.B. et al. Noninsulinoma pancreatogenous hypoglycemia: a novel syndrome of hyperinsulinemic hypoglycemia in adults independent of mutations in Kir6.2 and SUR1 genes. J Clin Endocrinol Metab. 1999; 84: 1582-1589 PubMed Google Scholar ), plasma glucagon did increase in response to food deprivation. Thus, the deficient response of glucagon in patients with insulinoma is specific for hypoglycemia. On the basis of the 5th percentile response concentration, the authors concluded that a value ≤10 pg/ml might indicate glucagon deficiency." @default.
• W2461964768 created "2016-07-22" @default.
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• W2461964768 date "2003-03-01" @default.
• W2461964768 modified "2023-09-24" @default.
• W2461964768 title "Establishing the Deficiency of Glucagon Response to Hypoglycemia in Humans" @default.
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• W2461964768 doi "https://doi.org/10.4158/ep.9.2.164" @default.
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