首页> 美国卫生研究院文献>Scientific Reports >Dietary fibers inhibit obesity in mice but host responses in the cecum and liver appear unrelated to fiber-specific changes in cecal bacterial taxonomic composition
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Dietary fibers inhibit obesity in mice but host responses in the cecum and liver appear unrelated to fiber-specific changes in cecal bacterial taxonomic composition

机译:膳食纤维可抑制小鼠的肥胖但盲肠和肝脏中的宿主反应似乎与盲肠细菌分类学组成中的纤维特异性变化无关

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摘要

Dietary fibers (DF) can prevent obesity in rodents fed a high-fat diet (HFD). Their mode of action is not fully elucidated, but the gut microbiota have been implicated. This study aimed to identify the effects of seven dietary fibers (barley beta-glucan, apple pectin, inulin, inulin acetate ester, inulin propionate ester, inulin butyrate ester or a combination of inulin propionate ester and inulin butyrate ester) effective in preventing diet-induced obesity and links to differences in cecal bacteria and host gene expression. Mice (n = 12) were fed either a low-fat diet (LFD), HFD or a HFD supplemented with the DFs, barley beta-glucan, apple pectin, inulin, inulin acetate ester, inulin propionate ester, inulin butyrate ester or a combination of inulin propionate ester and inulin butyrate ester for 8 weeks. Cecal bacteria were determined by Illumina MiSeq sequencing of 16S rRNA gene amplicons. Host responses, body composition, metabolic markers and gene transcription (cecum and liver) were assessed post intervention. HFD mice showed increased adiposity, while all of the DFs prevented weight gain. DF specific differences in cecal bacteria were observed. Results indicate that diverse DFs prevent weight gain on a HFD, despite giving rise to different cecal bacteria profiles. Conversely, common host responses to dietary fiber observed are predicted to be important in improving barrier function and genome stability in the gut, maintaining energy homeostasis and reducing HFD induced inflammatory responses in the liver.
机译:膳食纤维(DF)可以防止高脂饮食(HFD)喂养的啮齿动物肥胖。他们的作用方式尚未完全阐明,但肠道菌群已被牵连。这项研究旨在确定有效预防饮食的七种膳食纤维(大麦β-葡聚糖,苹果果胶,菊粉,菊粉乙酸酯,菊粉丙酸酯,菊粉丁酸酯或菊粉丙酸酯和菊粉丁酸酯的组合)的作用。导致肥胖,并与盲肠细菌和宿主基因表达的差异有关。给小鼠(n = 12)喂低脂饮食(LFD),HFD或补充了DF的HFD,大麦β-葡聚糖,苹果果胶,菊粉,菊粉乙酸酯,菊粉丙酸酯,菊粉丁酸酯或将菊粉丙酸酯和菊粉丁酸酯联合使用8周。通过Illumina MiSeq测序确定16S rRNA基因扩增子的盲肠细菌。干预后评估宿主反应,身体成分,代谢标记和基因转录(盲肠和肝脏)。 HFD小鼠显示肥胖增加,而所有DF均阻止体重增加。在盲肠细菌中观察到DF特异性差异。结果表明,尽管产生了不同的盲肠细菌特征,但不同的DF阻止了HFD的体重增加。相反,预计对食物纤维的常见宿主反应在改善肠的屏障功能和基因组稳定性,维持能量稳态以及减少肝脏中HFD引起的炎症反应中很重要。

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