4.7 Article

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

期刊

FOOD & FUNCTION
卷 13, 期 9, 页码 4977-4992

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ROYAL SOC CHEMISTRY
DOI: 10.1039/d1fo04075h

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资金

  1. Science and Technology Innovation Program of Hunan Province [2020RC2062]
  2. National Natural Science Foundation of China [32172761]
  3. Hunan Province Forestry Science and Technology Special Project [XLK202101-1]

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This study found that Camellia seed oil can improve dyslipidemia and lipid accumulation in mice fed a high-fat diet through the reorganization of gut microbiota. Camellia oil supplementation regulates the composition and functional profiling of gut microbiota, increases the abundance of beneficial bacteria, and reduces lipid levels in serum and liver. Furthermore, Camellia oil supplementation inhibits the mTOR signaling pathway.
Camellia (Camellia oleifera 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 Dubosiella, Lactobacillus, and Alistipes 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, Alistipes and Dubosiella, mediated the inhibition of the mTOR pathway.

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