Bray G A, Goodman H M
J Lipid Res. 1968 Nov;9(6):714-9.
Epinephrine increases the oxidation of glucose in adipose tissue even when its lipolytic effects are markedly reduced or abolished by propranolol, nicotinic acid, ouabain, or thyroidectomy. In order to locate the site(s) at which epinephrine stimulates glucose utilization, we studied the effects of epinephrine on the oxidation of various metabolites of glucose. Epinephrine neither increased the production of (14)CO(2) from 1- or 3-(14)C-pyruvate nor affected pyruvate conversion to glyceride-glycerol. To assess the possibility that epinephrine might accelerate the entry of glucose into adipocytes, we studied the accumulation of the nonmetabolized sugar l-arabinose in the intracellular water of adipose tissue. Epinephrine increased arabinose penetration into adipocytes to a degree comparable with that caused by 0.1 mU/ml of insulin. Virtually identical results were obtained in tissues from thyroidectomized rats in which the lipolytic effects of epinephrine were significantly reduced. It is concluded that epinephrine increases glucose oxidation by promoting its entry into adipose tissue and that the effect is independent of lipolysis.
即使肾上腺素的脂解作用被普萘洛尔、烟酸、哇巴因或甲状腺切除显著降低或消除，它仍能增加脂肪组织中葡萄糖的氧化。为了确定肾上腺素刺激葡萄糖利用的位点，我们研究了肾上腺素对葡萄糖各种代谢物氧化的影响。肾上腺素既没有增加1-或3-(14)C-丙酮酸生成(14)CO(2)的量，也没有影响丙酮酸向甘油酯甘油的转化。为了评估肾上腺素可能加速葡萄糖进入脂肪细胞的可能性，我们研究了非代谢性糖L-阿拉伯糖在脂肪组织细胞内水中的积累情况。肾上腺素使阿拉伯糖进入脂肪细胞的程度与0.1 mU/ml胰岛素所引起的程度相当。在肾上腺素脂解作用显著降低的甲状腺切除大鼠的组织中也获得了几乎相同的结果。得出的结论是，肾上腺素通过促进葡萄糖进入脂肪组织来增加葡萄糖氧化，且该作用与脂解作用无关。
