Leonetti F, Foniciello M, Iozzo P, Riggio O, Merli M, Giovannetti P, Sbraccia P, Giaccari A, Tamburrano G
Servizio Speciale Emergenze Metaboliche Cattedra di Gastroenterologia 2, Universita "La Sapienza," Rome, Italy.
Metabolism. 1996 May;45(5):606-10. doi: 10.1016/s0026-0495(96)90031-1.
Idiopathic reactive hypoglycemia (IRH) is responsible for postprandial hypoglycemia. Normal insulin secretion and reduced response of glucagon to acute hypoglycemia, but mostly increased insulin sensitivity, represent the metabolic features of this syndrome- The present study has two aims: first, to investigate the fate of glucose utilization inside the cells to assess whether increased glucose disposal in IRH is due to the oxidative and/or nonoxidative pathway; and second, to evaluate glucagon response to prolonged insulin-induced hypoglycemia. In eight patients with IRH and eight normal (N) subjects, we performed two studies on different days: (1) 120-minute euglycemic-hyperinsulinemic (1.0 mU . kg-1 . min-1 regular human insulin) clamp associated with indirect calorimetry; and (2) 180-minute hypoglycemic (2.22 to 2.49 mmo/L achieved through 0.85 mU . kg-1 . min-1 intravenous [IV] regular human insulin) clamp. The results showed an increased insulin-mediated glucose uptake in IRH (9.10 +/- 0.19 v 6.78 +/- 0.18 mg kg-1 . min-1, P < .005). Glucose oxidation was similar in IRH subjects and controls both in basal conditions (1.39 +/- 0.16 v 1.42 +/- 0.15 mg . kg-1 . min-1 and during the clamp studies (2.57 +/- 0.21 v 2.78 +/- 0.26 mg . kg-1 . min-1. In contrast, nonoxidative glucose disposal was significantly higher in IRH than in N subjects (6.53 +/- 0.30 v 4.00 +/- 0.21 mg . kg-1 . min-1, P < .001). During insulinization, fat oxidation was reduced slightly more in IRH than in control subjects. During the hypoglycemic clamp, a significant (P < .01) increase in plasma glucagon concentrations was observed in normal subjects as compared with baseline, whereas no change occurred in IRH patients. In conclusion, in IRH: (1) increased insulin-mediated glucose disposal is due to the increase of nonoxidative glucose metabolism; and (2) glucagon secretion has been confirmed to be inadequate. The increase of insulin sensitivity associated with a deficiency in glucagon secretion can widely explain the occurrence of hypoglycemia in the late postprandial phase.
特发性反应性低血糖（IRH）是餐后低血糖的原因。正常的胰岛素分泌以及胰高血糖素对急性低血糖反应的降低，但主要是胰岛素敏感性增加，代表了该综合征的代谢特征。本研究有两个目的：第一，研究细胞内葡萄糖利用的命运，以评估IRH中葡萄糖处置增加是否归因于氧化和/或非氧化途径；第二，评估胰高血糖素对胰岛素诱导的长期低血糖的反应。在8例IRH患者和8例正常（N）受试者中，我们在不同日期进行了两项研究：（1）120分钟的正常血糖-高胰岛素血症（1.0 mU·kg-1·min-1正规人胰岛素）钳夹联合间接测热法；（2）180分钟的低血糖（通过0.85 mU·kg-1·min-1静脉内[IV]正规人胰岛素实现2.22至2.49 mmol/L）钳夹。结果显示，IRH中胰岛素介导的葡萄糖摄取增加（9.10±0.19对6.78±0.18 mg·kg-1·min-1，P<.005）。在基础状态下（1.39±0.16对1.42±0.15 mg·kg-1·min-1）以及钳夹研究期间（2.57±0.21对2.78±0.26 mg·kg-1·min-1），IRH受试者和对照组的葡萄糖氧化相似。相比之下，IRH中非氧化葡萄糖处置显著高于N受试者（6.53±0.30对4.00±0.21 mg·kg-1·min-1，P<.001）。在胰岛素化期间，IRH中脂肪氧化的降低略多于对照组。在低血糖钳夹期间，与基线相比，正常受试者血浆胰高血糖素浓度显著（P<.01）升高，而IRH患者无变化。总之，在IRH中：（1）胰岛素介导的葡萄糖处置增加归因于非氧化葡萄糖代谢的增加；（2）已证实胰高血糖素分泌不足。胰岛素敏感性增加与胰高血糖素分泌不足可广泛解释餐后晚期低血糖的发生。
