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没食子醇可改善肥胖症状,促进脂肪组织产热,并调节 HFD 喂养小鼠肠道微生物组成。

Tyrosol Ameliorates the Symptoms of Obesity, Promotes Adipose Thermogenesis, and Modulates the Composition of Gut Microbiota in HFD Fed Mice.

机构信息

State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang, Jiangxi, 330047, China.

Jiangxi Provincial Key Laboratory of Preventive Medicine, School of Public Health, Nanchang University, Nanchang, Jiangxi, 330006, China.

出版信息

Mol Nutr Food Res. 2022 Aug;66(15):e2101015. doi: 10.1002/mnfr.202101015. Epub 2022 May 18.

Abstract

SCOPE

Tyrosol is one of the main polyphenolic compounds in extra virgin olive oil (EVOO) and its role in combating obesity is unknown. Thus, this study is designed to investigate the effect of tyrosol consumption on obesity and its underlying mechanisms in high-fat diet (HFD)-induced mice.

METHODS AND RESULTS

After supplementation with 0.2% (wt/wt) tyrosol for 16 weeks, the final body weight, and the levels of plasma triacylglycerol (TG), total cholesterol (TC), and fasting glucose are significantly decreased when compared with HFD group. Furthermore, tyrosol may act as a ligand which binds with nuclear hormone receptor peroxisome proliferator-activated receptor alpha (PPARα). Uncoupling protein 1 (UCP1), iodothyronine deiodinase 2 (DIO2), PPAR-γ coactivator-1α (PGC-1α), and PR domain containing 16 (PRDM16), the downstream genes of PPARα which are related to thermogenic function of adipocytes, are significantly increased in both brown adipose tissue (BAT) and inguinal white adipose tissue (iWAT) after tyrosol administration. In addition, tyrosol changes the community composition of gut microbiota, including decreasing the ratio of Firmicutes to Bacteroidetes, and increasing the relative abundance of family muribaculaceae, genus Blautia and Lachnospiraceae_bacterium_28_4.

CONCLUSION

Tyrosol consumption attenuates obesity and related symptoms in HFD-fed mice probably via the modulation of PPARα-thermogenesis and gut microbiota.

摘要

范围

酪醇是特级初榨橄榄油(EVOO)中主要的多酚化合物之一,其在对抗肥胖中的作用尚不清楚。因此,本研究旨在研究酪醇消耗对高脂肪饮食(HFD)诱导的肥胖小鼠的肥胖及其潜在机制的影响。

方法和结果

补充 0.2%(wt/wt)酪醇 16 周后,与 HFD 组相比,最终体重、血浆三酰甘油(TG)、总胆固醇(TC)和空腹血糖水平均显著降低。此外,酪醇可能作为一种配体与核激素受体过氧化物酶体增殖物激活受体α(PPARα)结合。解偶联蛋白 1(UCP1)、甲状腺素脱碘酶 2(DIO2)、过氧化物酶体增殖物激活受体γ共激活因子 1α(PGC-1α)和 PR 结构域包含 16(PRDM16),这些都是与脂肪细胞产热功能有关的 PPARα 的下游基因,在棕色脂肪组织(BAT)和腹股沟白色脂肪组织(iWAT)中,酪醇给药后均显著增加。此外,酪醇改变了肠道微生物群落的组成,包括降低厚壁菌门与拟杆菌门的比例,并增加了 muribaculaceae 科、Blautia 属和 Lachnospiraceae_bacterium_28_4 的相对丰度。

结论

酪醇消耗可能通过调节 PPARα-产热和肠道微生物群来减轻 HFD 喂养小鼠的肥胖及其相关症状。

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