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补充谷氨酸可调节低蛋白饮食断奶大鼠结肠和肝脏中的氮代谢。

Glutamate Supplementation Regulates Nitrogen Metabolism in the Colon and Liver of Weaned Rats Fed a Low-Protein Diet.

作者信息

Jiang Da, Zhang Jing, Ji Yun, Dai Zhaolai, Yang Ying, Wu Zhenlong

机构信息

State Key Laboratory of Animal Nutrition and Feed Science, China Agricultural University, Beijing 100193, China.

出版信息

Nutrients. 2025 Apr 26;17(9):1465. doi: 10.3390/nu17091465.

DOI:10.3390/nu17091465
PMID:40362775
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12073364/
Abstract

: Glutamate, a nutritionally non-essential amino acid, is a key intermediate in nitrogen metabolism. Despite more studies on its functional role in intestine health, it remains unknown how glutamate regulates nitrogen metabolism in animals fed a low-protein diet. : Herein, we investigated the effects of glutamate supplementation on colonic amino acid transport, barrier protein expression, microbiota alterations, fecal nitrogen emissions, hepatic amino acid transport, and protein synthesis in weaned rats. : We found that protein restriction diminished the mucus thickness, reduced goblet cell numbers, and the expression of , in the colon. In contrast, glutamate supplementation reversed these effects, increasing the colon length and enhancing the expression of ZO-1, Occludin, and Claudin-1 in the colon. At the genus level, glutamate increased the abundance of and . Additionally, glutamate supplementation resulted in an increased apparent nitrogen digestibility, reduced the ratio of fecal nitrogen to total nitrogen intake, and increased the ratio of fecal microbial nitrogen to total nitrogen intake. Protein restriction decreased the mRNA level of , , , and , and the protein level of p-mTOR, mTOR, p-mTOR/mTOR, and p-p70S6K/p70S6K as well as p-4EBP1/4EBP1 in the liver. These effects were reversed by glutamate supplementation. : In conclusion, glutamate supplementation upregulates amino acid transporters and barrier protein expression in the colon, modulates microbiota composition to reduce fecal nitrogen excretion, and enhances amino acid transport and protein synthesis in the liver by activating the mTOR/p70S6K/4EBP1 pathway, which influences nitrogen metabolism in weaned rats fed a low-protein diet.

摘要

谷氨酸是一种营养非必需氨基酸,是氮代谢的关键中间产物。尽管对其在肠道健康中的功能作用有更多研究,但谷氨酸如何调节低蛋白饮食动物的氮代谢仍不清楚。

在此,我们研究了补充谷氨酸对断奶大鼠结肠氨基酸转运、屏障蛋白表达、微生物群改变、粪便氮排放、肝脏氨基酸转运和蛋白质合成的影响。

我们发现蛋白质限制会降低结肠黏液厚度、减少杯状细胞数量以及相关蛋白的表达。相比之下,补充谷氨酸可逆转这些影响,增加结肠长度并增强结肠中紧密连接蛋白1(ZO-1)、闭合蛋白(Occludin)和 Claudin-1的表达。在属水平上,谷氨酸增加了特定菌属的丰度。此外,补充谷氨酸导致表观氮消化率提高,粪便氮与总氮摄入量的比值降低,粪便微生物氮与总氮摄入量的比值增加。蛋白质限制降低了肝脏中相关基因的mRNA水平以及磷酸化雷帕霉素靶蛋白(p-mTOR)、雷帕霉素靶蛋白(mTOR)、p-mTOR/mTOR和磷酸化核糖体蛋白S6激酶(p-p70S6K)/p70S6K以及磷酸化真核翻译起始因子4E结合蛋白1(p-4EBP1)/4EBP1的蛋白水平。这些影响通过补充谷氨酸得以逆转。

总之,补充谷氨酸可上调结肠中氨基酸转运体和屏障蛋白的表达,调节微生物群组成以减少粪便氮排泄,并通过激活mTOR/p70S6K/4EBP1途径增强肝脏中的氨基酸转运和蛋白质合成,从而影响低蛋白饮食断奶大鼠的氮代谢。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/f128c7f8c857/nutrients-17-01465-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/ce7ed76489cf/nutrients-17-01465-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/c6a1434d0742/nutrients-17-01465-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/5e4e669a048d/nutrients-17-01465-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/553ba8caa43e/nutrients-17-01465-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/e4ef371a2de4/nutrients-17-01465-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/e26a0200d548/nutrients-17-01465-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/7f50f12a8779/nutrients-17-01465-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/f128c7f8c857/nutrients-17-01465-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/ce7ed76489cf/nutrients-17-01465-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/c6a1434d0742/nutrients-17-01465-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/5e4e669a048d/nutrients-17-01465-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/553ba8caa43e/nutrients-17-01465-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/e4ef371a2de4/nutrients-17-01465-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/e26a0200d548/nutrients-17-01465-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/7f50f12a8779/nutrients-17-01465-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fc7/12073364/f128c7f8c857/nutrients-17-01465-g008.jpg

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