Lack of soluble fiber drives diet-induced adiposity in mice.
Lack of soluble fiber drives diet-induced adiposity in mice.
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DOI：
10.1152/ajpgi.00172.2015
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发表时间：
2015-10-01
期刊：
影响因子：
--
通讯作者：
Gewirtz AT
中科院分区：
文献类型：
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作者：
Chassaing B;Miles-Brown J;Pellizzon M;Ulman E;Ricci M;Zhang L;Patterson AD;Vijay-Kumar M;Gewirtz AT
饮食诱导的肥胖通常通过比较喂食高脂饮食（HFD）的小鼠来建模，高脂饮食（HFD）由纯化成分制成，而正常食物饮食（NCD）是相对未精制的植物和动物产品的低脂组合。HFD促进肥胖的机制很复杂，但被认为涉及低度炎症和改变的肠道微生物群。本研究的目的是研究HFD诱导的肥胖在多大程度上是由脂肪含量与区分HFD与NCD的其他因素驱动的。给小鼠喂食NCD、HFD或其他成分确定的饮食（CDD），其设计用于模拟NCD和/或探索HFD组分的作用。一系列反映低度炎症和肥胖的代谢参数进行了测定。相对于NCD、HFD，尽管程度较小，但在很大程度上，CDD诱导了肥胖增加，这表明脂质含量和HFD的其他方面都是致肥胖的。此外，HFD和CDD引起盲肠和结肠质量的快速和显着的损失。这种CD诱导的影响不受影响，通过调整膳食蛋白质水平/类型，但可以在很大程度上消除交换可溶性纤维（菊粉）的不溶性纤维（纤维素）。在HFD中用菊粉代替纤维素也可以保护小鼠免受肠质量减少、摄食过多和肥胖增加的影响。菊糖的这种有益作用是微生物群依赖性的，与通过基于1H-NMR的代谢组学分析的粪便短链脂肪酸水平升高相关，并且通过施用短链脂肪酸部分重现。HFD诱导的肥胖症由于其缺乏可溶性纤维而强烈促进，可溶性纤维支持微生物群介导的肠组织稳态，从而防止炎症驱动肥胖症和代谢综合征。
Diet-induced obesity is often modeled by comparing mice fed high-fat diet (HFD), which is made from purified ingredients, vs. normal chow diet (NCD), which is a low-fat assemblage of relatively unrefined plant and animal products. The mechanism by which HFD promotes adiposity is complex but thought to involve low-grade inflammation and altered gut microbiota. The goal of this study was to investigate the extent to which HFD-induced adiposity is driven by fat content vs. other factors that differentiate HFD vs. NCD. Mice were fed NCD, HFD, or other compositionally defined diets (CDD), designed to mimic NCD and/or explore the role of HFD components. A range of metabolic parameters reflecting low-grade inflammation and adiposity were assayed. Relative to NCD, HFD, and to a lesser, but, nonetheless, significant extent, CDD induced increased adiposity, indicating both lipid content and other aspects of HFD are obesogenic. Moreover, HFD and CDD induced a rapid and marked loss of cecal and colonic mass. Such CDD-induced effects were not affected by adjusting dietary protein levels/types but could be largely eliminated by exchanging insoluble fiber (cellulose) for soluble fiber (inulin). Replacing cellulose with inulin in HFD also protected mice against decreased intestinal mass, hyperphagia, and increased adiposity. Such beneficial effects of inulin were microbiota dependent, correlated with elevated fecal short-chain fatty acid levels analyzed via 1H-NMR-based metabolomics and were partially recapitulated by administration of short-chain fatty acid. HFD-induced obesity is strongly promoted by its lack of soluble fiber, which supports microbiota-mediated intestinal tissue homeostasis that prevents inflammation driving obesity and metabolic syndrome.