These findings suggest that KDC and FBT could attenuate features of the metabolic syndrome in HFD-fed mice, which might be due to the modulation of gut microbiota by KDC and FBT.

An increasing amount of evidence suggests that the gut microbiota composition and structure contribute to the pathophysiology of metabolic syndrome (MS), which has been put forward as a new target in the treatment of diet-induced MS. In this work, we aimed to investigate effects of Fuzhuan brick tea polysaccharides (FBTPS) on MS and gut microbiota dysbiosis in high-fat diet (HFD) fed mice and to further investigate whether its attenuation of MS is related to the modulation of gut microbiota. The results showed that FBTPS intervention could significantly attenuate metabolic syndrome in HFD-induced mice. Based on results of sequencing, FBTPS treatment could increase the phylogenetic diversity of HFD-induced microbiota. FBTPS intervention could significantly restore the HFD-induced increases in relative abundances of Erysipelotrichaceae, Coriobacteriaceae, and Streptococcaceae. Spearman's correlation analysis showed that 44 key OTUs were negatively or positively associated with MS. Our results suggested that FBTPS could serve as a novel candidate for prevention of MS in association with the modulation of gut microbiota.

Objective: To investigate and compare the effects of two common dietary phytosterols, stigmasterol and β-sitosterol, in altering lipid metabolism and attenuating nonalcoholic fatty liver disease (NAFLD). Methods: Stigmasterol and β-sitosterol were administered to mice at 0.4% in a high-fat western-style diet (HFWD) for 17 weeks. Results: Stigmasterol and β-sitosterol significantly ameliorated HFWD-induced fatty liver and metabolic abnormalities, including elevated levels of hepatic total lipids, triacylglycerols, cholesterol and liver histopathology. Both phytosterols decreased the levels of intestinal bile acids, accompanied by markedly increased fecal lipid levels. In addition, they altered the expression of genes involved in lipid metabolism. β-Sitosterol was less effective in affecting most of these parameters. Lipidomic analysis of liver and serum samples showed that stigmasterol prevented the HFWD-induced elevation of some di- and triacylglycerol species and lowering of some phospholipid species. Stigmasterol also decreased serum levels of ceramides. Conclusion: Stigmasterol and β-sitosterol, at a dose corresponding to that suggested for humans by the FDA for lowering cholesterol levels, are shown to alleviate HFWD-induced NAFLD. Stigmasterol was more effective than β-sitosterol, possibly because of its suppression of hepatic lipogenic gene expression and modulation of circulating ceramide levels.

EGCG decreases bile acid reabsorption, results in lower intestinal bile acid levels, which further decreases the absorption of lipids. These actions contribute to the alleviation of metabolic abnormalities and fatty liver disease caused by the high-fat diet.

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To study the effects of stigmasterol and β-sitosterol on high-fat Western diet (HFWD)-induced nonalcoholic fatty liver disease (NAFLD), lipidomic analyses were conducted in liver samples collected after 33 weeks of the treatment. Principal component analysis showed these phytosterols were effective in protecting against HFWD-induced NAFLD. Orthogonal projections to latent structures-discriminate analysis (OPLS-DA) and S-plots showed that triacylglycerols (TGs), phosphatidylcholines, cholesteryl esters, diacylglycerols, and free fatty acids (FFAs) were the major lipid species contributing to these discriminations. The alleviation of NAFLD is mainly associated with decreases in hepatic cholesterol, TGs with polyunsaturated fatty acids, and alterations of free hepatic FFA. In conclusion, phytosterols, at a dose comparable to that suggested for humans by the FDA for the reduction of plasma cholesterol levels, are shown to protect against NAFLD in this long-term (33-week) study.

Phytosterols, the plant analogues of cholesterol, widely occur in the human diet. In this study, we investigated and compared the effects of stigmasterol and β-sitosterol (both with purities ≥ 95%) on dextran sulfate sodium (DSS)-induced colitis in C57BL/6J male mice fed a high fat western-style diet. Mice treated with DSS developed severe mucosal colitis, with a marked distortion and crypt loss of colonic surface epithelium. Both β-sitosterol and stigmasterol significantly inhibited colon shortening, lowered fecal hemoglobin contents, and reduced the severity of colitis in the middle and distal colon (p < 0.05). They also significantly suppressed the activation of inflammatory master regulator nuclear factor-kappa B. Stigmasterol significantly lowered colonic inflammation score and the expression of cyclooxygenase-2 and colony stimulating factor-1, while β-sitosterol was less or not effective. These results suggest that dietary intake of stigmasterol and β-sitosterol ameliorate colitis. Such activities of stigmasterol and β-sitosterol in humans remain to be investigated.

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