Suppr超能文献

[肠道的氨和谷氨酰胺代谢。乳果糖和新霉素的作用]

[Ammonia and glutamine metabolism of the intestine. The effect of lactulose and neomycin].

作者信息

Soeters P B, van Leeuwen P A

出版信息

Infusionsther Klin Ernahr. 1986 Aug;13(4):186-90.

PMID:3759231
Abstract

The present work is directed to distinguish between ammonia production by the mucosa and by the intestinal flora, as well as to evaluate the influence of neomycin and lactulose. In vitro studies using rat intestine show that mucosa cells produce ammonia alanine and glutamic acid when incubated with glutamine, whose process can be impaired by neomycin or lactulose. Since the release of the above solutes is virtually the same in germ-free rats, the influence of the bacterial flora might be negligible under the experimental conditions used. Elimination of the aerobic microorganisms results in a minute decrease of ammonia concentration in portal blood in contrast to elimination of the anaerobic flora, which leads to an excessive reduction of ammonia formation. In germ-free rats colonisation with anaerobic microorganisms results in an increment in portal ammonia concentration, whose value, however, is still below levels observed in normal animals. Colonisation with aerobic bacteria has no effect on portal ammonia concentration. Neomycin and lactulose affect ammonia production in the gut by interfering with glutamine uptake in the mucosa cell, thus the influence upon ammonia formation apparently can not be exclusively explained by alterations of the intestinal flora. Possible reasons for the considerable increase in arterial glutamine levels in normal rats are discussed.

摘要

本研究旨在区分黏膜和肠道菌群产生氨的情况,以及评估新霉素和乳果糖的影响。使用大鼠肠道进行的体外研究表明,黏膜细胞在与谷氨酰胺一起孵育时会产生氨、丙氨酸和谷氨酸,新霉素或乳果糖会损害这一过程。由于在无菌大鼠中上述溶质的释放基本相同,在所使用的实验条件下,细菌菌群的影响可能微不足道。与消除厌氧菌群导致氨生成过度减少相反,消除需氧微生物会使门静脉血中氨浓度略有下降。在无菌大鼠中,厌氧微生物定殖会导致门静脉氨浓度升高,但其值仍低于正常动物中观察到的水平。需氧细菌定殖对门静脉氨浓度没有影响。新霉素和乳果糖通过干扰黏膜细胞对谷氨酰胺的摄取来影响肠道中的氨生成,因此对氨形成的影响显然不能仅通过肠道菌群的改变来解释。文中讨论了正常大鼠动脉谷氨酰胺水平显著升高的可能原因。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验