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血管加压素对灌注小鼠肝脏中脂肪酸合成的抑制作用及对糖原分解的刺激作用。

Inhibition of fatty acid synthesis and stimulation of glycogen breakdown by vasopressin in the perfused mouse liver.

作者信息

Ma G Y, Hems D A

出版信息

Biochem J. 1975 Nov;152(2):389-92. doi: 10.1042/bj1520389.

Abstract
  1. Vasopressin (anti-diuretic hormone, [8-arginine]vasopressin) inhibited the synthesis de novo of fatty acids (measured with (3)H(2)O and U-(14)C-labelled lactate or U-(14)C-labelled glucose) and stimulated glycogen breakdown in the perfused liver of fed mice. 2. The concentration dependence of these effects (range 200-1000muunits/ml, i.e. 0.5-2.5ng/ml) resembled that for the action on glycogen breakdown which was previously reported for rat liver. 3. The appearance of newly synthesized fatty acids in both phospholipids and triglycerides was inhibited by vasopressin, whereas synthesis of cholesterol was less affected. 4. Inhibition of hepatic lipogenesis by vasopressin is the most potent short-term hormonal action on this process yet reported. Aspects of the effect are discussed, including the lack of a role for cyclic AMP, and a possible link with vasopressin action on glycogen metabolism.
摘要
  1. 血管加压素(抗利尿激素,[8-精氨酸]血管加压素)抑制了脂肪酸的从头合成(用³H₂O和U-¹⁴C标记的乳酸或U-¹⁴C标记的葡萄糖进行测定),并刺激了喂食小鼠灌注肝脏中的糖原分解。2. 这些作用的浓度依赖性(范围为200 - 1000微单位/毫升,即0.5 - 2.5纳克/毫升)类似于先前报道的对大鼠肝脏糖原分解的作用。3. 血管加压素抑制了磷脂和甘油三酯中新合成脂肪酸的出现,而胆固醇的合成受影响较小。4. 血管加压素对肝脏脂肪生成的抑制是迄今为止报道的对该过程最有效的短期激素作用。讨论了该作用的各个方面,包括环磷酸腺苷的作用缺失以及与血管加压素对糖原代谢作用的可能联系。

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