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茶多酚通过调节高脂饮食诱导小鼠的肠道微生物群-短链脂肪酸-屏障和炎症来减轻肥胖。

Tea Polyphenols Reduced Obesity by Modulating Gut Microbiota-SCFAs-Barrier and Inflammation in High-Fat Diet-Induced Mice.

作者信息

Tian Baoming, Huang Pinjiao, Pan Yizhu, Gu Hong, Yang Kai, Wei Zhengxun, Zhang Xiangchun

机构信息

College of Food Science and Technology, Zhejiang University of Technology, Huzhou, 313299, China.

Tea Research Institute, Chinese Academy of Agricultural Sciences, Hangzhou, 310018, China.

出版信息

Mol Nutr Food Res. 2024 Dec;68(24):e2400685. doi: 10.1002/mnfr.202400685. Epub 2024 Nov 22.

Abstract

SCOPE

Obesity by high-fat diets (HFDs) is a chronic metabolic disorder that poses a significant threat to human health. Tea polyphenols (TPs) can prevent obesity caused by HFD by modulating gut microbiota.

METHODS AND RESULTS

To explore the function of TP in mitigating the effects of obesity and inflammation, mice are fed HFDs either with or without TP. TP supplementation effectively attenuates HFD-induced weight gain, liver and adipose tissue accumulation, while also improving liver fat content as well as colon and ileum tissue morphology. TP supplementation leads to a downregulation of lipid accumulation genes and an upregulation of lipid-decomposition genes. Moreover, TP increases Blautia and Faecalibaculum while reducing the Colidextribacter and short-chain fatty acids in HFD-induced mice, significantly activates G protein-coupled receptors, inhibits histone deacetylases, enhances intestinal tight junction expression levels, reduces intestinal permeability, and thereby preserves intestinal barrier integrity. Additionally, TP markedly suppresses the expression of inflammatory cytokines and inhibits the activation of TLR4 signaling pathways.

CONCLUSION

These findings suggest that TP holds great promise for improving both obesity management and alleviating intestinal inflammation, and provides a clue for understanding the antiobesity effects of TP.

摘要

范围

高脂饮食(HFD)导致的肥胖是一种慢性代谢紊乱,对人类健康构成重大威胁。茶多酚(TP)可通过调节肠道微生物群预防高脂饮食引起的肥胖。

方法与结果

为探究TP在减轻肥胖和炎症影响方面的作用,给小鼠喂食含或不含TP的高脂饮食。补充TP可有效减轻高脂饮食诱导的体重增加、肝脏和脂肪组织堆积,同时还能改善肝脏脂肪含量以及结肠和回肠组织形态。补充TP会导致脂质积累基因下调,脂质分解基因上调。此外,TP可增加高脂饮食诱导小鼠体内的布劳特氏菌属和粪杆菌属,同时减少柯林斯氏菌属和短链脂肪酸,显著激活G蛋白偶联受体,抑制组蛋白脱乙酰酶,提高肠道紧密连接表达水平,降低肠道通透性,从而维持肠道屏障完整性。此外,TP可显著抑制炎性细胞因子的表达,并抑制TLR4信号通路的激活。

结论

这些发现表明,TP在改善肥胖管理和减轻肠道炎症方面具有巨大潜力,并为理解TP的抗肥胖作用提供了线索。

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