Diamant S, Shafrir E
Eur J Biochem. 1975 May 6;53(2):541-6. doi: 10.1111/j.1432-1033.1975.tb04097.x.
Administration of triamcinolone or dexamethasone to rats led to a prompt, marked and persistent rise in liver acetyl-CoA carboxylase activity. The activity of fatty acid synthetase increased to a lesser extent and after a more prolonged glucocorticoid treatment, whereas the changes in that of NADP-malate dehydrogenase and ATP-citrate lyase were not appreciable. The overall channeling of [1-14-C]acetyl-CoA to fatty acids was enhanced. The triamcinolone effect on acetyl-CoA carboxylase activity appeared to be dependent on the coincident hyperinsulinemia since it was not obtained in alloxan-diabetic rats, whereas the alanine-aminotransferase-inducing effect of this hormone was additive to that of insulin deficiency. In adipose tissue triamcinolone treatment caused a reduction in the activity of all lipogenesis enzymes and blunted their response to insulin administration. The antagonism of glucocorticoids toward insulin, selectively modulating the responses of the insulin-sensitive enzymes in liver and adipose tissue is discussed. The rise in hepatic lipogenic capacity, through the retention of the ability of insulin to induce acetyl-CoA carboxylase, may be physiologically important in restraining the ketogenesis from acetyl-CoA despite the increased fat utilization during glucocorticoid excess.
给大鼠注射曲安奈德或地塞米松会导致肝脏乙酰辅酶A羧化酶活性迅速、显著且持续升高。脂肪酸合成酶的活性升高幅度较小，且在更长时间的糖皮质激素治疗后才出现，而NADP-苹果酸脱氢酶和ATP-柠檬酸裂解酶的变化不明显。[1-14-C]乙酰辅酶A向脂肪酸的整体转运增强。曲安奈德对乙酰辅酶A羧化酶活性的影响似乎依赖于同时存在的高胰岛素血症，因为在四氧嘧啶糖尿病大鼠中未观察到这种影响，而该激素诱导丙氨酸转氨酶的作用与胰岛素缺乏的作用是相加的。在脂肪组织中，曲安奈德治疗导致所有脂肪生成酶的活性降低，并减弱了它们对胰岛素给药的反应。讨论了糖皮质激素对胰岛素的拮抗作用，即选择性调节肝脏和脂肪组织中胰岛素敏感酶的反应。尽管在糖皮质激素过量期间脂肪利用率增加，但通过保留胰岛素诱导乙酰辅酶A羧化酶的能力，肝脏脂肪生成能力的提高在抑制由乙酰辅酶A生成酮体方面可能具有重要的生理意义。
