Benson J W, Johnson D G, Palmer J P, Werner P L, Ensinck J W
J Clin Endocrinol Metab. 1977 Mar;44(3):459-64. doi: 10.1210/jcem-44-3-459.
To examine the role of catecholamines in glucopenia-induced glucagon secretion, urinary epinephrine and norepinephrine and plasma immunoreactive glucagon (IRG) were measured during insulin-induced hypoglycemia in normal and insulin-dependent diabetic-man. Despite equivalent levels of hypoglycemia the mean plasma IRG increment in diabetes was only 15% of normals. The increases in epinephrine and norepinephrine were comparable in diabetics and normals; thus, the blunted response in plasma IRG to the stimulus of low blood sugar in diabetics cannot be explained by a generalized defect in catecholamine secretion. It is suggested that an alpha-cell glucoreceptor defect may account for the abnormal response to glucopenia in diabetics. To evaluate the possibility that impaired sensitivity to circulating catecholamines could explain the alpha cell dysfunction in diabetics, exogenous epinephrine was infused in normals and insulin-dependent diabetics. Elevated plasma IRG during epinephrine infusion was observed in only 50% of normals. The diabetics were hyperresponsive; mean increment in plasma IRG 3 times that of normals. The data demonstrate enhanced rather than impaired sensitivity to catecholamines in diabetes mellitus.
为研究儿茶酚胺在低血糖诱导的胰高血糖素分泌中的作用，我们测定了正常人和胰岛素依赖型糖尿病患者在胰岛素诱导低血糖期间的尿肾上腺素、去甲肾上腺素以及血浆免疫反应性胰高血糖素（IRG）。尽管低血糖水平相当，但糖尿病患者血浆IRG的平均增量仅为正常人的15%。糖尿病患者和正常人的肾上腺素和去甲肾上腺素增加量相当；因此，糖尿病患者血浆IRG对低血糖刺激反应迟钝不能用儿茶酚胺分泌的普遍缺陷来解释。有人提出，α细胞葡萄糖受体缺陷可能是糖尿病患者对低血糖异常反应的原因。为评估对循环儿茶酚胺敏感性受损是否能解释糖尿病患者的α细胞功能障碍，我们对正常人和胰岛素依赖型糖尿病患者输注外源性肾上腺素。肾上腺素输注期间，仅50%的正常人血浆IRG升高。糖尿病患者反应过度；血浆IRG的平均增量是正常人的3倍。数据表明，糖尿病患者对儿茶酚胺的敏感性增强而非受损。
