Koerker D J, Halter J B
Am J Physiol. 1982 Sep;243(3):E225-33. doi: 10.1152/ajpendo.1982.243.3.E225.
Glucose production decreases markedly following acute reduction in insulin and glucagon secretion (induced by somatostatin). After about an hour, however, glucose production is restored nearly to basal rates. To study the mechanism by which this occurs, islet hormone deficiency was superimposed on beta-adrenergic blockade. It was found that the hypoglycemia that accompanies insulin and glucagon deficiency is an adequate stimulus for catecholamine secretion. During combined hormone deficiency and beta-blockade, glucose production fell and remained very low for 2-3 h. This resulted in a profound hypoglycemia (glucose less than 30 mg/dl). We conclude from these studies that restoration of glucose production during sustained insulin and glucagon deficiency is not attributable to a) onset of insulin deficiency because insulin is equally depressed in both experimental settings, b) glucose autoregulation even though adequate substrate is available, or c) an alpha-adrenergic mechanism because plasma catecholamines were very high and alpha-receptors were not blocked. Rather, the glucose counterregulation during insulin and glucagon deficiency must be heavily dependent on a beta-adrenergic mechanism.
在胰岛素和胰高血糖素分泌急性减少（由生长抑素诱导）后，葡萄糖生成显著降低。然而，大约一小时后，葡萄糖生成几乎恢复到基础水平。为了研究这种情况发生的机制，将胰岛激素缺乏与β-肾上腺素能阻断叠加。发现伴随胰岛素和胰高血糖素缺乏的低血糖是儿茶酚胺分泌的充分刺激因素。在激素联合缺乏和β-阻断期间，葡萄糖生成下降并在2 - 3小时内维持在非常低的水平。这导致了严重的低血糖（血糖低于30mg/dl）。我们从这些研究中得出结论，在持续的胰岛素和胰高血糖素缺乏期间葡萄糖生成的恢复并非归因于：a）胰岛素缺乏的开始，因为在两种实验情况下胰岛素均同等程度地受到抑制；b）葡萄糖自身调节，即使有足够的底物；或c）α-肾上腺素能机制，因为血浆儿茶酚胺非常高且α-受体未被阻断。相反，胰岛素和胰高血糖素缺乏期间的葡萄糖反向调节必须严重依赖于β-肾上腺素能机制。
