血管加压素、血管紧张素II和去氧肾上腺素对肝脏生酮作用及脂肪酸合成的影响。

Effects of vasopressin, angiotensin II and phenylephrine on hepatic ketogenesis and fatty acid synthesis.

作者信息

Nomura T, Tachibana M, Maekawa H, Nomura H, Izuhara K, Hagino Y

出版信息

Jpn J Pharmacol. 1986 Aug;41(4):525-32. doi: 10.1254/jjp.41.525.

DOI:10.1254/jjp.41.525

Abstract

Studies were conducted to clarify the effects of vasopressin, angiotensin II and phenylephrine on hepatic ketogenesis and fatty acid synthesis. Hepatocytes from fed rats were incubated with oleate or octanoate. Vasopressin stimulated fatty acid synthesis as well as lactate and pyruvate accumulation in the presence of oleate. In accordance with this action, vasopressin caused a marked decrease in ketogenesis from oleate. When octanoate was added as a substrate, vasopressin failed to inhibit ketogenesis. Neither angiotensin II nor phenylephrine affected ketogenesis or fatty acid synthesis. The results in the present study show that there are vasopressin-mediated reciprocal changes in ketogenesis from oleate and fatty acid synthesis in isolated hepatocytes.

摘要

开展了多项研究以阐明血管加压素、血管紧张素 II 和去氧肾上腺素对肝脏生酮作用及脂肪酸合成的影响。将喂食大鼠的肝细胞与油酸或辛酸一起孵育。在油酸存在的情况下，血管加压素刺激脂肪酸合成以及乳酸和丙酮酸的积累。与此作用一致，血管加压素导致油酸生酮作用显著降低。当添加辛酸作为底物时，血管加压素未能抑制生酮作用。血管紧张素 II 和去氧肾上腺素均未影响生酮作用或脂肪酸合成。本研究结果表明，在分离的肝细胞中，存在血管加压素介导的油酸生酮作用和脂肪酸合成的相互变化。