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山茶( bel.)籽油通过 mTOR 通路重编程肠道微生物群,缓解高脂肪喂养小鼠的脂质积累。

Camellia ( bel.) seed oil reprograms gut microbiota and alleviates lipid accumulation in high fat-fed mice through the mTOR pathway.

机构信息

Research Institute of Oil Tea Camellia, Hunan Academy of Forestry, Shao shan South Road, No. 658, Changsha 410004, China.

National Engineering Research Center for Oil Tea Camellia, Changsha 410004, China.

出版信息

Food Funct. 2022 May 10;13(9):4977-4992. doi: 10.1039/d1fo04075h.

DOI:10.1039/d1fo04075h
PMID:35452062
Abstract

Camellia ( bel.) seed oil (CO) is extensively used as an edible oil in China and Asian countries owing to its high nutritional and medicinal values. It has been shown that a high-fat diet enhances lipid accumulation and induces intestinal microbiota imbalance in mice. However, it is still to be learned whether CO prevents dyslipidemia through gut microbiota. Here, using 16S rRNA gene sequencing analysis of the gut microbiota, we found that oral CO relieved lipid accumulation and reversed gut microbiota dysbiosis. Compared to mice (C57BL/6J male mice) fed a high-fat diet, treatment with CO regulated the composition and functional profiling communities related to the lipid metabolism of gut microbiota. The abundances of , , and were markedly increased in CO supplementation mice. In addition, the colon levels of isobutyric acid, pentanoic acid, and isovaleric acid were similar between the control and CO supplementation mice. Besides, the results indicated that CO supplementation in mice alleviated lipid droplet accumulation in the hepatocytes and subcutaneous adipose tissue, although the liver index did not show a difference. Notably, CO supplementation for 6 weeks significantly reduced the levels of LDL, TC, and TG, while enhancing the level of HDL in serum and liver. Meanwhile, we also identified that CO supplementation suppressed the mammalian target of rapamycin (mTOR) signaling pathway in high fat-fed (HF-fed) mice. Taken together, our results suggest that CO improved dyslipidemia and alleviated lipid accumulation in HF-fed mice, the molecular mechanisms possibly associated with the reorganization of gut microbiota, in particular, and , mediated the inhibition of the mTOR pathway.

摘要

油茶籽油(CO)在中国和亚洲国家被广泛用作食用油,因为它具有很高的营养价值和药用价值。研究表明,高脂肪饮食会促进脂肪积累,并导致小鼠肠道微生物群落失衡。然而,CO 是否通过肠道微生物群预防血脂异常仍有待研究。在这里,我们通过对肠道微生物群的 16S rRNA 基因测序分析发现,口服 CO 可缓解脂质积累并逆转肠道微生物群失调。与高脂肪饮食喂养的小鼠(C57BL/6J 雄性小鼠)相比,CO 处理调节了与肠道微生物群脂质代谢相关的组成和功能特征群落。在 CO 补充组中, 、 和 的丰度明显增加。此外,CO 补充组小鼠结肠中异丁酸、戊酸和异戊酸的水平与对照组相似。此外,结果表明 CO 补充剂可减轻肝细胞和皮下脂肪组织中的脂肪滴积累,尽管肝指数没有差异。值得注意的是,CO 补充剂可显著降低血清和肝脏中 LDL、TC 和 TG 的水平,同时提高 HDL 的水平。同时,我们还发现 CO 补充剂可抑制高脂肪饮食喂养(HF 喂养)小鼠中的哺乳动物雷帕霉素靶蛋白(mTOR)信号通路。综上所述,我们的结果表明,CO 改善了 HF 喂养小鼠的血脂异常和脂质积累,其分子机制可能与肠道微生物群的重新组织有关,特别是 和 ,介导了 mTOR 通路的抑制。

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