PANCREATIC ALPHA-CELL FUNCTION IN IDIOPATHIC REACTIVE HYPOGLYCEMIA

Idiopathic reactive hypoglycemia (IRH) is a well-documented but overdi agnosed syndrome. The presence of transient hypoglycemia and enhanced insulin secretion and/or increased insulin sensitivity before the onse t of IRH is well documented, However, the data regarding glucagon secr etion are sparse. Therefore, this study assessed glucagon and insulin responses to (1) oral ingestion of 100 g glucose oral glucose toleranc e test (OGTT) and (2) a 100-g protein meal after an overnight fast in a randomized sequence at intervals of 7 to 10 days in five subjects wi th previously well-documented IRH and six normal subjects. Basal plasm a glucose and insulin levels were not significantly different in both groups. However, basal glucagon was significantly higher (P < .025) in IRH subjects (347 +/- 83 ng/L) compared with normals (135 +/- 20 ng/L ). In IRH subjects during the OGTT, hypoglycemia (2.7 +/- 0.11 mmol/L) occurred at 150 +/- 16 minutes and was preceded by a markedly higher (P < .01) peak glucose concentration (11.7 +/- 0.6 mmol/L) at 36 +/- 6 minutes in comparison to normals (8.8 +/- 0.4 mmol/L), indicating the presence of impaired glucose tolerance in these subjects. Similarly, the plasma insulin increase was significantly higher (P < .01) but del ayed in IRH subjects compared with normals. In contrast, glucagon supp ression was not significantly different in both groups, although gluca gon failed to increase following hypoglycemia in IRH. During a protein meal, plasma glucose declined in both groups, with a significantly (P < .05) greater decrease in IRH subjects (-0.8 +/- 0.2 mmol/L) compare d with normals (0.5 +/- 0.1 mmol/L). However, the glucagon increase wa s significantly (P < .01) blunted in IRH subjects (61% +/- 15%) in com parison to normals (152% +/- 39%), Thus, basal hyperglucagonemia with normal glucose concentration may suggest the presence of a hyposensiti vity of the glucagon receptor in IRH. Moreover, the lack of appropriat e suppression during the OGTT despite marked hyperglycemia, the lack o f an increase at the onset of hypoglycemia, and the inhibited response to a protein meal in IRH subjects compared with normals denote altere d glucagon secretion in IRH. Therefore, it is likely that glucagon rec eptor downregulation and impaired glucagon sensitivity and secretion m ay contribute to postprandial hypoglycemia in IRH. Copyright (C) 1997 by W.B. Saunders Company.