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Microalgae oil from Schizochytrium sp. alleviates obesity and modulates gut microbiota in high-fat diet-fed mice

文献类型： 外文期刊

作者： Ran, Liyuan 1 ; Yu, Jinhui 2 ; Ma, Rui 2 ; Yao, Qing 2 ; Wang, Mingjie 5 ; Bi, Yuping 4 ; Yu, Zichao 1 ; Wu, Yingjie 1 ;

作者机构： 1.Shandong First Med Univ & Shandong Acad Med Sci, Shandong Prov Hosp, Coll Lab Anim, Shandong Lab Anim Ctr,Med Sci & Technol Innovat Ct, Jinan 250117, Peoples R China

2.Dalian Med Univ, Inst Genome Engn Anim Models Human Dis, Dalian 116044, Peoples R China

3.Dalian Med Univ, Natl Ctr Genet Engn Anim Models Int Res, Dalian 116044, Peoples R China

4.Shandong Acad Agr Sci, Inst Crop Germplasm Resources, Jinan 250100, Peoples R China

5.Shandong Univ, Shandong Prov Hosp, Jinan, Peoples R China

6.Inner Mongolia Med Univ, Affiliated Hosp, Dept Endocrinol, Inner Mongolia, Peoples R China

期刊名称：FOOD & FUNCTION （ 影响因子：6.317； 五年影响因子：6.375 ）

ISSN： 2042-6496

年卷期： 2022 年 13 卷 24 期

页码：

收录情况： SCI

摘要： Omega-3 PUFAs rich in fish oil are believed to prevent obesity by improving lipid metabolism and regulating gut microbiota. Microalgae oil is considered as an alternative source of omega-3 PUFAs owing to diminishing fish resources. Schizochytrium microalgae oil (SMO), with a high DHA proportion, is a promising source for commercial DHA production. However, its weight-loss and gut microbiota-regulating properties are not well studied. Here we compared the obesity reducing effects of SMO, commercial fish oil (FO) and a weight-loss drug, Orlistat (OL), in a high-fat diet (HFD) induced obesity mouse model. We found that SMO is comparable to commercial FO and OL with regard to weight loss, and it even exhibits the weight-loss effects earlier than FO and OL. It can efficiently inhibit the expression of lipogenesis-related genes and induce the expression of lipolysis-related genes. Moreover, SMO has different gut microbiota modulating effects from those of FO and OL. It does not influence the diversity of bacterial community, but does increase the abundance of several beneficial SCFAs-producing bacteria and inhibits obesity-promoting Desulfovibrio and several pathogens. We also found that SMO recovers the HFD-disturbed metabolic capability of gut microbiota. It can increase the abundance of several metabolism-related pathways, such as those of amino acids, SCFAs and bile acid, and decrease the level of the LPS biosynthesis pathway, which probably contributes to an improvement of lipid metabolism and restoration of the colonic mucosal barrier impaired by HFD. Our data suggest that SMO can be used as a superior dietary supplement for alleviating obesity.

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