4.7 Article

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

期刊

FOOD & FUNCTION
卷 13, 期 24, 页码 12799-12813

出版社

ROYAL SOC CHEMISTRY
DOI: 10.1039/d2fo01772e

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资金

  1. Ministry of Science and Technology (National Key R&D Program of China) [2021YFA0805100, 2021YFF0702100]
  2. National Science Foundation of China [31871163, 81600668]
  3. Research Project of the Education Department of Liaoning [LZ2020046]

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Omega-3 PUFAs rich in fish oil are believed to prevent obesity by improving lipid metabolism and regulating gut microbiota. Microalgae oil, particularly Schizochytrium microalgae oil (SMO) with a high DHA proportion, is shown to have comparable weight-loss effects to commercial fish oil and a weight-loss drug. In addition, SMO has different effects on gut microbiota, increasing the abundance of beneficial bacteria and inhibiting obesity-promoting bacteria. SMO also helps restore the disturbed metabolic capability of gut microbiota caused by a high-fat diet.
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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