HORMONAL MECHANISMS OF RECOVERY FROM INSULIN-INDUCED HYPOGLYCEMIA IN MAN
HORMONAL MECHANISMS OF RECOVERY FROM INSULIN-INDUCED HYPOGLYCEMIA IN MAN
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DOI：
10.1152/ajpendo.1979.236.4.e380
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发表时间：
1979-01-01
影响因子：
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通讯作者：
CRYER, P
中科院分区：
文献类型：
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作者：
GERICH, J;DAVIS, J;CRYER, P
在正常和肾上腺切除的人类受试者中，研究了使用生长抑素抑制胰高血糖素和生长激素[GH]分泌，从急性胰岛素诱导的低血糖中恢复血糖的机制。在胰高血糖素和生长激素缺乏的正常受试者中，输注生长抑素增强胰岛素诱导的血糖下降，尽管血浆皮质醇、肾上腺素和去甲肾上腺素反应增强，但却减弱了正常血糖的恢复;这些作用可通过同时输注生长抑素和胰高血糖素（生长激素缺乏的受试者）而非生长激素（胰高血糖素缺乏的受试者）来预防。在接受糖皮质激素替代（肾上腺素缺乏症）的肾上腺切除受试者中，胰岛素给药后的血糖反应与正常受试者无显著差异;然而，生长抑素输注（肾上腺素、胰高血糖素和GH缺乏症）增强了这些受试者中胰岛素诱导的低血糖，并且完全消除了正常血糖的恢复。在人类急性胰岛素诱导的低血糖中，胰高血糖素起主要作用，肾上腺素起次要作用。生长激素、皮质醇或神经释放的去甲肾上腺素的直接作用未被指出。
Mechanisms for recovery of plasma glucose from acute insulin-induced hypoglycemia were investigated in normal and adrenalectomized human subjects with somatostatin used to inhibit glucagon and growth hormone [GH] secretion. In normal subjects with glucagon and GH deficiency, infusion of somatostatin enhanced insulin-induced plasma glucose decrements and attenuated restitution of normoglycemia despite augmented plasma cortisol, epinephrine and norepinephrine responses; these effects were prevented by simultaneous infusion of somatostatin with glucagon (subjects with GH deficiency) but not with GH (subjects with glucagon deficiency). In adrenalectomized subjects receiving glucocorticoid replacement (epinephrine deficiency), plasma glucose responses after insulin administration were not significantly different from those of normal subjects; however, somatostatin infusion (epinephrine, glucagon and GH deficiency) enhanced insulin-induced hypoglycemia more in these subjects than in the normal subjects and completely abolished restitution of normoglycemia. Glucagon plays a primary role and epinephrine a secondary role in recovery of plasma glucose from acute insulin-induced hypoglycemia in man. The immediate contributions of growth hormone, cortisol or neurally released norepinephrine were not indicated.