Werner P L, Benson J W, Brodsky J B, Hollander P M, Asplin C M, Johnson D G, Palmer J P
Am J Physiol. 1980 Sep;239(3):E227-31. doi: 10.1152/ajpendo.1980.239.3.E227.
2-Deoxy-D-glucose (2DG), by competitive inhibition of glucose utilization, produces a state of intracellular glucopenia with resultant activation of both the sympathetic and parasympathetic branches of the autonomic nervous system. We have investigated the relationship between the activation of the autonomic nervous system caused by this drug and glucagon secretion. Subjects experienced symptoms identical to those observed during true hypoglycemia and demonstrated a marked rise in both gastric acid secretion and urinary epinephrine excretion. Mean immunoreactive glucagon (IRG) levels rose only slightly post-2DG (maximal mean increment, 18 pg/ml). Insulin-induced hypoglycemia, although eliciting a similar increase in urinary epinephrine excretion, was followed by a severalfold increase in IRG. Thus, although hypoglycemia and 2DG induced similar discharge of the autonomic nervous system, the glucagon response to hypoglycemia was much greater. These observations provide strong evidence that marked increases in sympathetic and parasympathetic discharge in man are weak alpha-cell stimuli and further support the hypothesis that the rise in IRG that occurs during hypoglycemia is not mediated primarily via the autonomic nervous system.
2-脱氧-D-葡萄糖（2DG）通过竞争性抑制葡萄糖利用，产生细胞内低血糖状态，从而导致自主神经系统的交感和副交感分支均被激活。我们研究了这种药物引起的自主神经系统激活与胰高血糖素分泌之间的关系。受试者出现了与真正低血糖期间观察到的症状相同的症状，并且胃酸分泌和尿肾上腺素排泄均显著增加。2DG给药后，平均免疫反应性胰高血糖素（IRG）水平仅略有上升（最大平均增量为18 pg/ml）。胰岛素诱导的低血糖虽然引起尿肾上腺素排泄有类似增加，但随后IRG会增加数倍。因此，尽管低血糖和2DG诱导了类似的自主神经系统放电，但胰高血糖素对低血糖的反应要大得多。这些观察结果提供了有力证据，表明人体交感和副交感神经放电的显著增加是较弱的α细胞刺激因素，并进一步支持了以下假设：低血糖期间发生的IRG升高并非主要通过自主神经系统介导。
