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- W4386547162 endingPage "1882" @default.
- W4386547162 startingPage "1882" @default.
- W4386547162 abstract "Gut dysbiosis has been associated with many chronic diseases, such as obesity, inflammatory bowel disease, and cancer. Gut dysbiosis triggers these diseases through the activation of the immune system by the endotoxins produced by gut microbiota, which leads to systemic inflammation. In addition to pre-/pro-/postbiotics, many natural products can restore healthy gut microbiota composition. Tocotrienol, which is a subfamily of vitamin E, has been demonstrated to have such effects. This scoping review presents an overview of the effects of tocotrienol on gut microbiota according to the existing scientific literature. A literature search to identify relevant studies was conducted using PubMed, Scopus, and Web of Science. Only original research articles which aligned with the review's objective were examined. Six relevant studies investigating the effects of tocotrienol on gut microbiota were included. All of the studies used animal models to demonstrate that tocotrienol altered the gut microbiota composition, but none demonstrated the mechanism by which this occurred. The studies induced diseases known to be associated with gut dysbiosis in rats. Tocotrienol partially restored the gut microbiota compositions of the diseased rats so that they resembled those of the healthy rats. Tocotrienol also demonstrated strong anti-inflammatory effects in these animals. In conclusion, tocotrienol could exert anti-inflammatory effects by suppressing inflammation directly or partially by altering the gut microbiota composition, thus achieving its therapeutic effects." @default.
- W4386547162 created "2023-09-09" @default.
- W4386547162 creator A5004770379 @default.
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- W4386547162 creator A5085765991 @default.
- W4386547162 creator A5092827022 @default.
- W4386547162 date "2023-09-07" @default.
- W4386547162 modified "2023-10-17" @default.
- W4386547162 title "The Effects of Tocotrienol on Gut Microbiota: A Scoping Review" @default.
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