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白藜芦醇对高脂饮食诱导的肥胖小鼠脂肪代谢和肠道微生物群的调节作用

Modulation of fat metabolism and gut microbiota by resveratrol on high-fat diet-induced obese mice.

作者信息

Campbell C Linda, Yu Renqiang, Li Fengzhi, Zhou Qin, Chen Daozhen, Qi Ce, Yin Yongxiang, Sun Jin

机构信息

State Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi 214122, China.

School of Food Science and Technology, Jiangnan University, Wuxi 214122, China.

出版信息

Diabetes Metab Syndr Obes. 2019 Jan 4;12:97-107. doi: 10.2147/DMSO.S192228. eCollection 2019.

DOI:10.2147/DMSO.S192228
PMID:30655683
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6324607/
Abstract

PURPOSE

The antioxidant resveratrol (RSV) has low bioavailability and can reach the colon to access the gut microbial ecosystem. RSV administration together with high-fat diet prevented abnormal changes of intestinal microbiota. However, whether or not RSV can reshape the intestinal microbiota of obese mice and alleviate obesity-related diseases remains to be studied. This study aimed to explore the role of RSV in alleviating high-fat-induced obesity and its relationship with oxidative stress and gut microbiota.

METHODS

Male C57BL/6 mice were divided into five groups and administered for 16 weeks with: standard diet (CON), high-fat diet (60% energy for lard, HFD), and HFD with low, medium, and high dose of RSV, 50, 75, and 100 mg/kg body weight administered daily via drinking water, respectively.

RESULTS

Medium and high RSV treatment significantly prevented body weight gain, decreased relative weight of liver and adipose tissue compared with HFD (<0.05). All doses significantly prevented HFD-induced increase of serum triglyceride, low density lipoprotein cholesterol, glucose, and endotoxemia (<0.05). Medium and high dose also prevented chronic inflammation by decreasing serum interleukin-1 and tumor necrosis factor-alpha (<0.05), and oxidative stress in liver and brain indicated by increase in superoxide dismutase, catalase, glutathione peroxidase activity (<0.05). Formation of malondialdehyde was prevented by all doses compared with HFD (<0.05). Both medium and high doses of RES increased alpha diversity of gut microbiota according to the Chao1 and Shannon indices (<0.05). Medium dose induced obvious shift in gut microbiota composition according to principal component analysis. High dose of RSV effectively prevented HFD-induced increase of Coriobacteriaceae and Desulfovi-brionaceae (<0.05), which show a significant correlation with body weight (>0.8 <0.00).

CONCLUSION

RSV prevented HFD-induced endotoxemia, oxidative stress, and gut microbiota change.

摘要

目的

抗氧化剂白藜芦醇(RSV)生物利用度低,可到达结肠并进入肠道微生物生态系统。给予RSV并搭配高脂饮食可预防肠道微生物群的异常变化。然而,RSV是否能重塑肥胖小鼠的肠道微生物群并减轻肥胖相关疾病仍有待研究。本研究旨在探讨RSV在减轻高脂诱导的肥胖中的作用及其与氧化应激和肠道微生物群的关系。

方法

将雄性C57BL/6小鼠分为五组,并分别给予16周的以下处理:标准饮食(CON)、高脂饮食(60%能量来自猪油,HFD),以及添加低、中、高剂量RSV的高脂饮食,分别通过饮用水每日给予50、75和100mg/kg体重。

结果

与高脂饮食组相比,中、高剂量RSV处理显著预防了体重增加,降低了肝脏和脂肪组织的相对重量(<0.05)。所有剂量均显著预防了高脂饮食诱导的血清甘油三酯、低密度脂蛋白胆固醇、血糖和内毒素血症的增加(<0.05)。中、高剂量还通过降低血清白细胞介素-1和肿瘤坏死因子-α预防了慢性炎症(<0.05),并通过超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶活性的增加表明预防了肝脏和大脑中的氧化应激(<0.05)。与高脂饮食组相比,所有剂量均预防了丙二醛的形成(<0.05)。根据Chao1和香农指数,中、高剂量的RES均增加了肠道微生物群的α多样性(<0.05)。根据主成分分析,中剂量诱导了肠道微生物群组成的明显变化。高剂量的RSV有效预防了高脂饮食诱导的科里杆菌科和脱硫弧菌科的增加(<0.05),这与体重呈显著正相关(>0.8 <0.00)。

结论

RSV预防了高脂饮食诱导的内毒素血症、氧化应激和肠道微生物群变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/4b2ff8404306/dmso-12-097Fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/7d3051c1f53d/dmso-12-097Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/f5d3e1d8e0f1/dmso-12-097Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/654697938a23/dmso-12-097Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/2dc9c73ba9bd/dmso-12-097Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/8d378b1b6c79/dmso-12-097Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/a11fefb699bf/dmso-12-097Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/4b2ff8404306/dmso-12-097Fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/7d3051c1f53d/dmso-12-097Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/f5d3e1d8e0f1/dmso-12-097Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/654697938a23/dmso-12-097Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/2dc9c73ba9bd/dmso-12-097Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/8d378b1b6c79/dmso-12-097Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/a11fefb699bf/dmso-12-097Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebbb/6324607/4b2ff8404306/dmso-12-097Fig7.jpg

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