Abstract
Flaxseed (Linum usitatissimum L.) is known as healthy food for its anti-obesity and lipid modulating properties. However, the effects of flaxseed polysaccharide (FSP) on metabolic syndrome (MetS) and gut microbiota are still poorly understood. Here, we investigated the effects of FSP on lipid metabolism and gut microbiota in high-fat diet-fed mice. FSP effectively reduced the serum fasting glucose, total triglyceride and total cholesterol levels. FSP consumption adipose accumulation impacted the gut microbiome at different taxonomic levels by increasing the proportions of beneficial Akkermansia and Bifidobacterium and decreasing the disease or obesity associated Oscillospira and Odoribacteraceae. These changes were highly correlated with the regulation of expression levels of lipid metabolism involved genes in the liver. The restoration of total SCFAs, especially propionate and butyrate might be an important strategy for mitigating HFD induced metabolic disorders. These findings suggest that FSP may use as a prebiotic for preventing MetS by modulating the gut microbiota.
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Key Points
Reports have shown that polysaccharides as dietary fiber could be good candidates for attenuating MetS by modulating the gut microbe composition, modifying the lipid metabolism and immunomodulatory activities. The effect of FSP on gut microbiota and the possible mechanism between the modulation of gut microbiota and MetS remains unclear. In this study, the effect of FSP supplementation on MetS and gut microbiota dysbiosis in HFD mice were investigated. Lipid metabolism related genes, specific responded gut microbiota and their metabolite SCFAs to HFD were analyzed to provide potential insights into FSP as a candidate prebiotics for preventing MetS.
Modulation of gut microbiota by FSP was found closely related with alleviation of the hyperglycemia and lipid metabolic disorder in serum. A strong regulation of host liver genes involved in lipid metabolism by FSP and the microbial metabolites propionate and butyrate. This is the first report of the proposed anti-MetS mechanism of FSP, thereby providing a comprehensive understanding of the interaction between polysaccharide and gut microbiota.
FSP supplementation partially restored the HFD-induced decrease in SCFAs, especially propionate and butyrate, to normal levels. These results corresponded to the upregulation of several SCFA producing bacteria, in the FSP-supplemented mice, including Prevotella, Roseburia and Anaerotruncus, of which were found tightly linked to energy metabolism. Fermentation of FSP to SCFAs by the gut microbiota may be an important strategy for mitigating obesity and its associated metabolic diseases. HFD induced MetS associated fat accumulation, glucose and TG levels were well controlled by the FSP treatments. Dietary supplementation of FSP also led to dramatic changes in gut microbial community structure, including a reduction in the ratio of Firmicutes to Bacteroidetes and a bloom of Akkermansia and Bifidobacterium. These changes, especially the proliferation of Akkermansia may partially associated with the regulation of lipid metabolism-related genes, thus confer some degree of protection from the negative consequences of an HFD. The restoration of total SCFAs and the increasing propionate and butyrate suggested it might be an important strategy for mitigating HFD induced metabolic disorders. The findings suggest that FSP may be used as a prebiotic for preventing MetS by modulating the gut microbiota.