Simonson D C, Koivisto V, Sherwin R S, Ferrannini E, Hendler R, Juhlin-Dannfelt A, DeFronzo R A
J Clin Invest. 1984 Jun;73(6):1648-58. doi: 10.1172/JCI111371.
We investigated the effects of alpha and/or beta adrenergic blockade (with phentolamine and/or propranolol) on glucose homeostasis during exercise in six normal subjects and in seven Type I diabetic subjects. The diabetics received a low dose insulin infusion (0.07 mU/kg X min) designed to maintain plasma glucose at approximately 150 mg/dl. In normals, neither alpha, beta, nor combined alpha and beta adrenergic blockade altered glucose production, glucose uptake, or plasma glucose concentration during exercise. In diabetics, exercise alone produced a decline in glucose concentration from 144 to 116 mg/dl. This was due to a slightly diminished rise in hepatic glucose production in association with a normal increase in glucose uptake. When exercise was performed during beta adrenergic blockade, the decline in plasma glucose was accentuated. An exogenous glucose infusion (2.58 mg/kg X min) was required to prevent glucose levels from falling below 90 mg/dl. The effect of beta blockade was accounted for by a blunted rise in hepatic glucose production and an augmented rise in glucose utilization. These alterations were unrelated to changes in plasma insulin and glucagon levels, which were similar in the presence and absence of propranolol. In contrast, when the diabetics exercised during alpha adrenergic blockade, plasma glucose concentration rose from 150 to 164 mg/dl. This was due to a significant increase in hepatic glucose production and a small decline in exercise-induced glucose utilization. These alterations also could not be explained by differences in insulin and glucagon levels. We conclude that the glucose homeostatic response to exercise in insulin-dependent diabetics, in contrast to healthy controls, is critically dependent on the adrenergic nervous system.
我们研究了α和/或β肾上腺素能阻断（使用酚妥拉明和/或普萘洛尔）对6名正常受试者和7名I型糖尿病受试者运动期间葡萄糖稳态的影响。糖尿病患者接受低剂量胰岛素输注（0.07 mU/kg×分钟），旨在将血浆葡萄糖维持在约150 mg/dl。在正常受试者中，单独的α、β或联合的α和β肾上腺素能阻断均未改变运动期间的葡萄糖生成、葡萄糖摄取或血浆葡萄糖浓度。在糖尿病患者中，单独运动使葡萄糖浓度从144 mg/dl降至116 mg/dl。这是由于肝脏葡萄糖生成的增加略有减少，同时葡萄糖摄取正常增加。当在β肾上腺素能阻断期间进行运动时，血浆葡萄糖的下降加剧。需要外源性葡萄糖输注（2.58 mg/kg×分钟）以防止葡萄糖水平降至90 mg/dl以下。β阻断的作用是由于肝脏葡萄糖生成的增加减弱以及葡萄糖利用的增加增强。这些改变与血浆胰岛素和胰高血糖素水平的变化无关，在有或没有普萘洛尔的情况下这些水平相似。相反，当糖尿病患者在α肾上腺素能阻断期间运动时，血浆葡萄糖浓度从150 mg/dl升至164 mg/dl。这是由于肝脏葡萄糖生成显著增加以及运动诱导的葡萄糖利用略有下降。这些改变也不能用胰岛素和胰高血糖素水平的差异来解释。我们得出结论，与健康对照相比，胰岛素依赖型糖尿病患者对运动的葡萄糖稳态反应严重依赖于肾上腺素能神经系统。
