Drost H, Grüneklee D, Kley H K, Wiegelmann W, Krüskemper H L, Gries F A
Klin Wochenschr. 1980 Nov 3;58(21):1197-205. doi: 10.1007/BF01478876.
Insulin-induced hypoglycemias are a sign of non-sufficient counterregulation, in which different contra-insulinary hormones participate. The aim of the study was to investigate, whether there exists a difference between IDD and non-diabetics regarding secretion of glucagon, cortisol, and growth hormone during an insulin-induced hypoglycemia and further on pointing out, expecially, the importance of glucagon. Insulin-induced hypoglycemias are counterregulated in non-diabetics, not in IDD. The missing glucagon secretion during insulin-induced hypoglycemia in IDD seems to be independent from an autonomic neuropathy. Only after high doses of exogenous glucagon can one see a counterregulating increase of glucose. The STH secretion is similar in non-diabetics and IDD during an insulin-induced hypoglycemia and has evidently only a secondary effect in hypoglycemic counterregulation. The STH secretion may be the expression of a diencephal-triggered stress situation. The cortisol secretion is the same in both groups. The gluconeogenetic effect of cortisol is not sufficient to accomplish a fast compensation of hypoglycemia. This does not exclude long-term effects. When inhibiting the secretion of insulin and different contra-insulinary hormones with somatostatin, one is able to demonstrate that glucagon alone is a sufficiently counterregulatory hormone in insulin-induced hypoglycemias.
胰岛素诱导的低血糖是反调节不足的一种表现，不同的抗胰岛素激素参与其中。本研究的目的是调查在胰岛素诱导的低血糖期间，1型糖尿病患者（IDD）与非糖尿病患者在胰高血糖素、皮质醇和生长激素分泌方面是否存在差异，并特别指出胰高血糖素的重要性。胰岛素诱导的低血糖在非糖尿病患者中可被反调节，但在1型糖尿病患者中则不然。1型糖尿病患者在胰岛素诱导的低血糖期间胰高血糖素分泌缺失似乎与自主神经病变无关。只有在给予高剂量外源性胰高血糖素后，才能观察到血糖的反调节性升高。在胰岛素诱导的低血糖期间，生长激素（STH）分泌在非糖尿病患者和1型糖尿病患者中相似，并且在低血糖反调节中显然仅起次要作用。生长激素分泌可能是间脑触发的应激状态的一种表现。两组的皮质醇分泌相同。皮质醇的糖异生作用不足以快速代偿低血糖。这并不排除长期影响。当用生长抑素抑制胰岛素和不同抗胰岛素激素的分泌时，能够证明在胰岛素诱导的低血糖中，单独胰高血糖素就是一种充分的反调节激素。
