EFFECT OF EPINEPHRINE ON GLUCOSE-METABOLISM IN HUMANS - CONTRIBUTION OF THE LIVER
EFFECT OF EPINEPHRINE ON GLUCOSE-METABOLISM IN HUMANS - CONTRIBUTION OF THE LIVER
复制标题
DOI：
10.1152/ajpendo.1984.247.2.e157
复制
发表时间：
1984-01-01
影响因子：
--
通讯作者：
SACCA, L
中科院分区：
文献类型：
--
作者：
SHERWIN, RS;SACCA, L
肾上腺素导致吸收后状态下血糖浓度迅速升高。这种作用是通过肝葡萄糖产生的短暂增加和胰岛素依赖性组织对葡萄糖处理的抑制来介导的。肾上腺素通过刺激糖原分解和糖异生来增加肝葡萄糖的产生。尽管肾上腺素对糖原分解的作用迅速减弱，但高血糖仍然存在，因为肾上腺素对糖异生和葡萄糖处理的作用持续存在。胰高血糖素和皮质醇同时升高或糖尿病患者会明显加剧肾上腺素引起的高血糖。在这两种情况下，肾上腺素对肝葡萄糖产生的影响从短暂的反应转变为持续的反应，从而解释了过度的高血糖。在葡萄糖喂养期间，肾上腺素轻度升高，对空腹血糖水平几乎没有影响，导致明显的葡萄糖不耐受。肾上腺素对糖尿病的作用如此敏感，是因为它能够干扰血糖调节反应的各个组成部分，即刺激内脏和外周葡萄糖摄取并抑制肝葡萄糖产生。我们的研究结果表明，肾上腺素是压力引起的高血糖和糖尿病患者对压力的不利代谢影响的易感性的重要因素。
Epinephrine causes a prompt increase in blood glucose concentration in the postabsorptive state. This effect is mediated by a transient increase in hepatic glucose production and an inhibition of glucose disposal by insulin-dependent tissues. Epinephrine augments hepatic glucose production by stimulating glycogenolysis and gluconeogenesis. Although its effect on glycogenolysis rapidly wanes, hyperglycemia continues because the effects of epinephrine on gluconeogenesis and glucose disposal persist. Epinephrine-induced hyperglycemia is markedly accentuated by concomitant elevations of glucagon and cortisol or in patients with diabetes. In both cases, the effect of epinephrine on hepatic glucose production is converted from a transient to a sustained response, thereby accounting for the exaggerated hyperglycemia. During glucose feeding, mild elevations of epinephrine that have little effect on fasting glucose levels cause marked glucose intolerance. This exquisite sensitivity to the diabetogenic effects of epinephrine is accounted for by its capacity to interfere with each of the components of the glucoregulatory response, i.e., stimulation of splanchnic and peripheral glucose uptake and suppression of hepatic glucose production. Our findings suggest that epinephrine is an important contributor to stress-induced hyperglycemia and the susceptibility of diabetics to the adverse metabolic effects of stress.