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叶酸缺乏对大鼠肠黏膜空肠转运的影响。

Effect of folate deficiency of the intestinal mucosa on jejunal transport in the rat.

作者信息

Goetsch C, Klipstein F A

出版信息

J Lab Clin Med. 1977 May;89(5):1002-8.

PMID:870567
Abstract

The role of folate deficiency in the pathogenesis of the abnormalities of structure and transport of the small intestine that are often present in certain disorders such as alcoholism is unclear. One reason for this is that the folate status of the intestinal mucosa has never been ascertained in humans. Previous investigations have shown that a deficient diet supplemented with sulfa does produce folate deficiency of the intestinal mucosa in weanling rats and that this is associated with diarrhea and structural abnormalities of the jejunum. In the present study, we used then in vivo marker perfusion technique to examine the jejunal transport of water, sodium, xylose, glucose, and L-leucine in such folate-deficient rats. Supplementation of the normal diet with sulfa did not produce folate deficiency of the intestinal mucosa, but it was associated with a moderate reduction in water absorption; this was attributed to cecal enlargement in these rats. Rats placed on a folate-deficient diet plus sulfa developed markedly depressed serum and jejunal folate concentrations, net secretion of water and sodium, and persistent diarrhea; absorption of xylose, glucose, and L-leucine remained normal, however. Folate repletion of these rats by water and sodium transport to absorption ano cessation of diarrhea. These observations indicate that folate deficiency of the intestinal mucosa alters the transport of water and electrolytes but not that of such solutes as xylose, glucose, and L-leucine. They suggest that when transport abnormalities of these solutes occur in folate-deficient alcoholics, this in not due to the folate deficiency but rather to other pathogenic factors such as ethanol.

摘要

叶酸缺乏在某些疾病(如酒精中毒)中常出现的小肠结构和转运异常的发病机制中所起的作用尚不清楚。原因之一是人类肠道黏膜的叶酸状态从未被确定过。先前的研究表明,用磺胺补充缺乏叶酸的饮食确实会使断奶大鼠的肠道黏膜出现叶酸缺乏,并且这与腹泻和空肠的结构异常有关。在本研究中,我们使用体内标记物灌注技术来检测此类叶酸缺乏大鼠空肠对水、钠、木糖、葡萄糖和L-亮氨酸的转运情况。用磺胺补充正常饮食并未导致肠道黏膜叶酸缺乏,但与水吸收的适度减少有关;这归因于这些大鼠的盲肠肿大。食用缺乏叶酸的饮食加磺胺的大鼠血清和空肠叶酸浓度显著降低,出现水和钠的净分泌以及持续腹泻;然而,木糖、葡萄糖和L-亮氨酸的吸收仍保持正常。给这些大鼠补充叶酸可使水和钠的转运恢复到吸收状态并停止腹泻。这些观察结果表明,肠道黏膜叶酸缺乏会改变水和电解质的转运,但不会改变木糖、葡萄糖和L-亮氨酸等溶质的转运。它们表明,当叶酸缺乏的酗酒者出现这些溶质的转运异常时,这并非由于叶酸缺乏,而是由于其他致病因素,如乙醇。

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