Pancreatic alpha-cell function in idiopathic reactive hypoglycemia
Pancreatic alpha-cell function in idiopathic reactive hypoglycemia
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DOI：
10.1016/s0026-0495(97)90006-8
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发表时间：
1997-06-01
影响因子：
9.8
通讯作者：
Kabadi, UM
中科院分区：
文献类型：
--
作者：
Ahmadpour, S;Kabadi, UM
特发性反应性低血糖症（IRH）是一种有据可查但被过度诊断的综合征。在IRH发作之前，短暂性低血糖和胰岛素分泌增强和/或胰岛素敏感性增加的存在是有据可查的，然而，关于胰高血糖素分泌的数据很少。因此，本研究评估了胰高血糖素和胰岛素对（1）口服摄入100 g葡萄糖口服葡萄糖耐量试验（OGTT）和（2）100 g蛋白质餐后过夜空腹在一个随机序列，间隔7至10天，在5名受试者与先前记录良好的IRH和6名正常受试者。两组的基础血糖和胰岛素水平无显著差异。然而，IRH受试者的基础胰高血糖素（347 +/- 83 ng/L）显著高于正常人（135 +/- 20 ng/L）（P <0.025）。在IRH受试者中，OGTT期间，低血糖（2.7 +/- 0.11 mmol/L）发生在150 +/- 16分钟，之前有明显较高的（P < .01）峰值葡萄糖浓度在36 +/- 6分钟时（11.7 +/- 0.6 mmol/L）与正常（8.8 +/- 0.4 mmol/L）相比，表明这些受试者中存在葡萄糖耐量受损。同样，与正常人相比，IRH受试者的血浆胰岛素升高显著更高（P <0.01），但延迟。相比之下，胰高血糖素抑制在两组中没有显著差异，尽管胰高血糖素在IRH中低血糖后未能增加。在蛋白质餐期间，两组的血浆葡萄糖均下降，IRH受试者（-0.8 +/-0.2 mmol/L）与正常人（0.5 +/-0.1 mmol/L）相比下降幅度更大（P <0.05）。然而，与正常人（152% +/-39%）相比，IRH受试者（61% +/-15%）中胰高血糖素的增加显著（P <0.01）减弱。因此，具有正常葡萄糖浓度的基础高胰高血糖素血症可能提示IRH中胰高血糖素受体的低敏感性。此外，尽管有明显的高血糖，但在OGTT期间缺乏适当的抑制，在低血糖发作时缺乏增加，以及与正常人相比，IRH受试者对蛋白质餐的反应受到抑制，表明IRH中胰高血糖素分泌的改变。因此，胰高血糖素受体下调和胰高血糖素敏感性和分泌受损可能导致IRH的餐后低血糖。版权所有（C）1997 W.B.桑德斯公司
Idiopathic reactive hypoglycemia (IRH) is a well-documented but overdiagnosed syndrome. The presence of transient hypoglycemia and enhanced insulin secretion and/or increased insulin sensitivity before the onset of IRH is well documented, However, the data regarding glucagon secretion are sparse. Therefore, this study assessed glucagon and insulin responses to (1) oral ingestion of 100 g glucose oral glucose tolerance 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 with previously well-documented IRH and six normal subjects. Basal plasma 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 delayed in IRH subjects compared with normals. In contrast, glucagon suppression was not significantly different in both groups, although glucagon 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) compared with normals (0.5 +/- 0.1 mmol/L). However, the glucagon increase was significantly (P < .01) blunted in IRH subjects (61% +/- 15%) in comparison to normals (152% +/- 39%), Thus, basal hyperglucagonemia with normal glucose concentration may suggest the presence of a hyposensitivity of the glucagon receptor in IRH. Moreover, the lack of appropriate suppression during the OGTT despite marked hyperglycemia, the lack of an increase at the onset of hypoglycemia, and the inhibited response to a protein meal in IRH subjects compared with normals denote altered glucagon secretion in IRH. Therefore, it is likely that glucagon receptor downregulation and impaired glucagon sensitivity and secretion may contribute to postprandial hypoglycemia in IRH. Copyright (C) 1997 by W.B. Saunders Company.