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Open Access Research Article Just Accepted
Protective effect of Fu Brick tea on high-fat diet-induced metabolic syndrome: Relevant to protecting the intestinal barrier and regulating the gut microbiota
Food Science and Human Wellness
Available online: 17 July 2024
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This study investigated the therapeutic effects on metabolic syndrome (MetS) and the impact on the intestinal barrier and gut microbiota of Fu brick tea aqueous extracts (FTE) on metabolic syndrome (MetS) in rats fed with a high-fat diet (HFD). Here, the results showed that FTE supplement significantly reduced HFD-induced weight gain, adiposity, dyslipidemia, fasting blood glucose (PBG) increment, and non-alcoholic fatty liver disease (NAFLD). Moreover, FTE supplement resulted in a decline in lipopolysaccharide (LPS) level and attenuation of colonic inflammation and oxidative stress to protect the intestinal barrier function. FTE supplement also maintained the intestinal barrier integrity by improving histological appearance and promoting ZO-1, Occludin, and Claudin-1 protein expression levels. Meanwhile, FTE supplement alleviated the gut microbiota dysbiosis by enhancing the Firmicutes/Bacteroidetes (F/B) ratio and stimulating the colonization of probiotic bacteria such as Akkermansia, Lactobacillus, Adlercreutzia, and Bacteroides. These findings collectively suggest that Fu brick tea could alleviate MetS and Mets-associated traits with the mechanism relevant to the protection of intestinal barrier and gut microbiota regulation.

Open Access Issue
Junshanyinzhen tea extract prevents obesity by regulating gut microbiota and metabolic endotoxemia in high-fat diet fed rats
Food Science and Human Wellness 2024, 13 (4): 2036-2047
Published: 20 May 2024
Abstract PDF (14.1 MB) Collect
Downloads:65

Obesity is associated with gut dysbiosis and metabolic endotoxin. Junshanyinzhen tea extract (JSTE) reduced fat accumulation and body weight in obese mice. However, the effects and mechanism of JSTE in preventing obesity were unclear. Therefore, we used different doses of JSTE (75, 150 and 300 mg/(kg·day)) to evaluate the effect on high-fat diet (HFD) -induced rats under 8 weeks of intervention. Here, our results showed that JSTE could significantly reduce body weight gain, blood lipid levels and fat accumulation, improve fatty damage in liver tissue (P < 0.05). In addition, JSTE increased the expression of intestinal tight junction proteins (P < 0.05), relieved metabolic endotoxemia (P < 0.05) and chronic low- grade inflammation in HFD rats. Sequencing of fecal samples showed that JSTE could effectively reverse the microbial diversity and the ratio of Firmicutes to Bacteroidetes to normal levels in HFD- fed rats. Desulfovibrioceae and Erysipelotrichaceae, which are positively related to obesity, were decreased by JSTE intervention (P < 0.05). while Bifidobacteriaceae, Bacteroidaceae, Akkermansia, and Clostridium, which are negatively related to obesity, were increased. Together, these results suggested that JSTE might effectively prevent obesity by modulating gut microbiota dysbiosis, intestinal barrier dysfunction, metabolic endotoxemia and chronic low-grade inflammation in HFD-induced rats.

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