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大鼠和狒狒长期摄入酒精后肝脏中α-氨基-n-丁酸生成增加。

Increased hepatic production of alpha-amino-n-butyric acid after chronic alcohol consumption in rats and baboons.

作者信息

Shaw S, Lieber C S

出版信息

Gastroenterology. 1980 Jan;78(1):108-13.

PMID:6765935
Abstract

Chronic alcohol consumption produces an increase in plasma alpha-amino-n-butyric acid (AANB) in humans. The mechanism of this increase was investigated in experimental animals. In the rat, administration of ethanol as 36% of total calories for 4--6 wk produced a threefold rise in plasma AANB associated with a sixfold increase in hepatic AANB. The increased gradient from liver to plasma suggested enhanced hepatic production. This was verified in liver slices from these animals: They showed a twofold increase in hepatic production of AANB. In the baboon, hepatic vein catheterization studies revealed a marked stimulation in splanchnic release of AANB after chronic but not acute alcohol consumption. Liver slices from these animals showed a two- to threefold increase in AANB production. Thus, increased hepatic production of AANB may explain the increased plasma levels seen in experimental animals and humans after chronic alcohol consumption.

摘要

长期饮酒会导致人体血浆α-氨基-n-丁酸(AANB)水平升高。在实验动物中对这种升高的机制进行了研究。在大鼠中,给予占总热量36%的乙醇,持续4至6周,会使血浆AANB升高三倍,同时肝脏AANB增加六倍。肝脏与血浆之间增加的梯度表明肝脏生成增强。这在这些动物的肝切片中得到证实:它们的肝脏AANB生成增加了两倍。在狒狒中,肝静脉插管研究显示,长期而非急性饮酒后,内脏对AANB的释放有明显刺激。这些动物的肝切片显示AANB生成增加了两到三倍。因此,肝脏AANB生成增加可能解释了实验动物和人类长期饮酒后血浆水平升高的现象。

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