Assimacopoulos-Jeannet F, Denton R M, Jeanrenaud B
Biochem J. 1981 Sep 15;198(3):485-90. doi: 10.1042/bj1980485.
The effect of vasopressin on the short-term regulation of fatty acid synthesis was studied in isolated hepatocytes from rats fed ad libitum. Vasopressin stimulates fatty acid synthesis by 30-110%. This increase is comparable with that obtained with insulin. Angiotensin also stimulates fatty acid synthesis, whereas phenylephrine does not. The dose-response curve for vasopressin-stimulated lipogenesis is similar to the dose-response curve for glycogenolysis and release of lactate plus pyruvate. Vasopression also stimulates acetyl-CoA carboxylase activity in a dose-dependent manner. Vasopressin does not relieve glucagon-inhibited lipogenesis, whereas insulin does. The action of vasopressin on hepatic lipogenesis is decreased, but not suppressed, in Ca2+-depleted hepatocytes. The results suggest that vasopressin acts on lipogenesis by increasing availability of lipogenic substrate (lactate + pyruvate) and by activating acetyl-CoA carboxylase.
在随意进食的大鼠分离肝细胞中研究了血管加压素对脂肪酸合成短期调节的作用。血管加压素可刺激脂肪酸合成增加30%-110%。这种增加与胰岛素所引起的增加相当。血管紧张素也刺激脂肪酸合成,而苯肾上腺素则无此作用。血管加压素刺激脂肪生成的剂量-反应曲线与糖原分解及乳酸加丙酮酸释放的剂量-反应曲线相似。血管加压素还以剂量依赖方式刺激乙酰辅酶A羧化酶活性。血管加压素不能解除胰高血糖素对脂肪生成的抑制作用,而胰岛素则可以。在钙离子缺乏的肝细胞中,血管加压素对肝脏脂肪生成的作用减弱,但未被抑制。结果表明,血管加压素通过增加脂肪生成底物(乳酸+丙酮酸)的可用性以及激活乙酰辅酶A羧化酶来作用于脂肪生成。