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PM 通过影响高碳水化合物饮食喂养的大鼠的肠道微生物群和代谢物诱导肠道损伤。

PM induces intestinal damage by affecting gut microbiota and metabolites of rats fed a high-carbohydrate diet.

机构信息

School of Chemistry and Chemical Engineering, Shihezi University, Key Laboratory of Environmental Monitoring and Pollutant Control of Xinjiang Bingtuan, Xinjiang, 832003, China.

Department of Endocrinology, Changji Branch, First Affiliated Hospital of Xinjiang Medical University, Xinjiang, 831100, China.

出版信息

Environ Pollut. 2021 Jun 15;279:116849. doi: 10.1016/j.envpol.2021.116849. Epub 2021 Mar 16.

DOI:10.1016/j.envpol.2021.116849
PMID:33773181
Abstract

PM has a major impact on the gastrointestinal system, but the specific mechanism behind this action is not fully understood. Current studies have focused on the relationship between PM and intestinal flora disorder, while ignoring the important influence of diet on gut microbes. In this study, SD rats were fed either a normal, high-fat, or high-carbohydrate diet for two months and exposed to PM (7 mg/kg b.w.) by intratracheal instillation. The results showed that the body and kidney weights of the rats in the high-fat diet group were significantly increased relative to those with a normal diet, and changes in the intestinal microbes and metabolites induced by PM were observed. Rats in the high-carbohydrate diet group had a significant response, and the diversity and richness indices of the flora were reduced (p < 0.05); additionally, intestinal Biffidobacterium and Lactobacillus were enriched, while many endogenous metabolites were found. Some amino acids derivatives and long-chain fatty acids were increased (p < 0.05). Both diet structure and PM exposure can affect the composition of gut microbiota, and intestinal metabolites may be associated with cell membrane damage when a high-carbohydrate diet interacts with PM. This study considers multiple dietary factors to further supplement the evidence of intestinal damage via PM.

摘要

PM 对胃肠道系统有重大影响,但这一作用的具体机制尚不完全清楚。目前的研究集中在 PM 与肠道菌群失调的关系上,而忽略了饮食对肠道微生物的重要影响。在这项研究中,SD 大鼠连续两个月分别给予正常饮食、高脂饮食或高碳水化合物饮食,并通过气管内滴注暴露于 PM(7mg/kg b.w.)。结果表明,与正常饮食组相比,高脂饮食组大鼠的体重和肾脏重量显著增加,并且观察到 PM 诱导的肠道微生物和代谢物发生变化。高碳水化合物饮食组大鼠反应明显,菌群的多样性和丰富度指数降低(p<0.05);此外,肠道双歧杆菌和乳酸杆菌得到富集,而许多内源性代谢物被发现。一些氨基酸衍生物和长链脂肪酸增加(p<0.05)。饮食结构和 PM 暴露均可影响肠道微生物群落的组成,而当高碳水化合物饮食与 PM 相互作用时,肠道代谢物可能与细胞膜损伤有关。本研究考虑了多种饮食因素,进一步补充了 PM 导致肠道损伤的证据。

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