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首页> 外文期刊>International Journal of Biological Macromolecules: Structure, Function and Interactions >Artemisia sphaerocephala Krasch polysaccharide mediates lipid metabolism and metabolic endotoxaemia in associated with the modulation of gut microbiota in diet-induced obese mice
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Artemisia sphaerocephala Krasch polysaccharide mediates lipid metabolism and metabolic endotoxaemia in associated with the modulation of gut microbiota in diet-induced obese mice

机译:Artemisia Sphaerocephala Krasch多糖在饮食诱导的肥胖小鼠中介导脂质代谢和代谢内毒素肿瘤的调节肠道微生物

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摘要

Artemisia sphaerocephala Krasch polysaccharide (ASKP) has been proved to have many bioactivities. To determine the underlying mechanisms on anti-obesogenic effect of ASKP in mice, parameters related to obesity, gut microbiota composition, and the correlation between the parameters and specific bacterial taxa were investigated. The results showed that ASKP significantly alleviated high-fat-diet-induced obesity in mice with the amelioration of dyslipidemia, and metabolic endotoxaemia. Relative expression analyses of genes indicated that ASKP administration modulated hepatic lipid metabolism with the downregulation of related genes, including ACC-1, FAS, SREBP-1c, and PPAR gamma. 16S rRNA analysis showed that ASKP mediated the gut dysbiosis induced by high-fat diet, such as the reduction of Proteobacteria, AF12, and Helicobacter. Spearman's correlation showed that some specific genera, such as Odoribacter, AF12, and Rikenella, were strongly associated with obesity-related parameters. Our results demonstrated that ASKP could serve as a potential prebiotic agent in the prevention of diet-induced obesity. (C) 2019 Elsevier B.V. All rights reserved.
机译:Artemisia Sphaerocephala Krasch多糖(ASKP)已被证明有许多生物活动。为了确定ASKP在小鼠中的抗噬菌体效果的潜在机制,研究了与肥胖,肠道微生物群组合物相关的参数和参数与特异性细菌分类基的相关性。结果表明,随着血脂血症的改善和代谢内毒性的改善,ASKP显着缓解了小鼠的高脂饮食诱导的肥胖症。基因的相对表达分析表明,ASKP给药调制肝脂质代谢与相关基因,包括ACC-1,FAS,SREBP-1c和PPAR伽马的下调。 16S rRNA分析显示,ASKP介导通过高脂饮食引起的肠道脱泻,例如蛋白细菌,AF12和幽灵的减少。 Spearman的相关性表明,一些特定的属,如臭氧,AF12和rikenella与肥胖相关参数强烈相关。我们的结果表明,ASKP可以作为预防饮食诱导的肥胖症的潜在益生元剂。 (c)2019 Elsevier B.v.保留所有权利。

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