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生物素缺乏雏鸡中乳酸盐的施用与脂肪肝和肾综合征的发展

Lactate administration and fatty liver and kidney syndrome development in biotin-deficient chicks.

作者信息

Balnave D, Pearce J

出版信息

Br Poult Sci. 1979 Jan;20(1):109-16. doi: 10.1080/00071667908416554.

Abstract

Two experiments were carried out to determine whether administration of lactate to biotin-deficient chicks induced fatty liver and kidney syndrome (FLKS). 2. The results suggest that increased serum lactate concentrations are a consequence of the syndrome rather than a contributory factor in its incidence. 3. The increase in liver lipids of birds affected by FLKS was not associated with an increase in the specific activity of the hepatic lipogenic enzyme acetyl CoA carboxylase accept when birds developed FLKS spontaneously in experiment 2. 4. Some biotin-deficient chicks did not show physical symptoms of deficiency although mean liver biotin concentrations were low (0.31 microgram/g liver).

摘要
  1. 进行了两项实验,以确定向生物素缺乏的雏鸡施用乳酸是否会诱发脂肪肝和肾综合征(FLKS)。2. 结果表明,血清乳酸浓度升高是该综合征的结果,而非其发病的促成因素。3. 受FLKS影响的鸟类肝脏脂质增加与肝脏脂肪生成酶乙酰辅酶A羧化酶的比活性增加无关,但在实验2中鸟类自发发生FLKS时除外。4. 一些生物素缺乏的雏鸡尽管肝脏生物素平均浓度较低(0.31微克/克肝脏),但未表现出缺乏的身体症状。

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