Propensity to high-fat diet-induced obesity in rats is associated with changes in the gut microbiota and gut inflammation
Propensity to high-fat diet-induced obesity in rats is associated with changes in the gut microbiota and gut inflammation
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DOI：
10.1152/ajpgi.00098.2010
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发表时间：
2010-08-01
影响因子：
4.5
通讯作者：
Raybould, Helen E.
中科院分区：
文献类型：
--
作者：
de La Serre, Claire Barbier;Ellis, Collin L.;Raybould, Helen E.
Barbier de la Serre C，Ellis CL，Lee J，Hartman AL，Rutledge JC，Raybould He。大鼠高脂饮食引起的肥胖症的倾向与肠道菌群和肠道炎症的变化有关。 Am J Physiol Gastrountest肝生理学299：G440-G448，2010年。首次发布于2010年5月27日； doi：10.1152/ajpgi.00098.2010。高脂肪和卡路里的饮食消费会导致肥大和肥胖，这与慢性“低度”全身炎症有关。摄入高脂饮食会改变肠道菌群，指出在肥胖发展中的作用。本研究使用sprague-dawley大鼠，当喂养高脂饮食时，表现出易肥胖（DIO-P）或抗肥胖症（dio-r）表型，以确定肠上皮功能的变化和微生物群的变化是饮食还是肥胖。每天在低脂肪饮食上维持的大鼠中，每天监测食物摄入量和体重。 8或12周后，去除组织以确定肥胖和肠上皮功能，并使用PCR分析肠道菌群。 DIO-P但非DiO-R大鼠表现出与回肠炎症相关的TOLL样受体（TLR4）激活的增加，并且肠道碱性磷酸酶（一种腔酶酶）的腔酶（一种对脂多糖酸（LPS）的解毒酶）。肠道通透性和血浆LPS与肌球蛋白轻链的磷酸化一起增加，并在上皮细胞的细胞质中定位。细菌16S rRNA的测量显示出总细菌密度的降低，无论表型如何，高脂喂养大鼠中细菌和梭状芽孢杆菌阶的相对比例的增加。仅在DIO-P大鼠的微生物群中看到肠杆菌的增加。高脂饮食的消费会引起肠道菌群的变化，但炎症的发展与应激症和肥胖表型有关。
Barbier de La Serre C, Ellis CL, Lee J, Hartman AL, Rutledge JC, Raybould HE. Propensity to high-fat diet-induced obesity in rats is associated with changes in the gut microbiota and gut inflammation. Am J Physiol Gastrointest Liver Physiol 299: G440-G448, 2010. First published May 27, 2010; doi: 10.1152/ajpgi.00098.2010.-Consumption of diets high in fat and calories leads to hyperphagia and obesity, which is associated with chronic "low-grade" systemic inflammation. Ingestion of a high-fat diet alters the gut microbiota, pointing to a possible role in the development of obesity. The present study used Sprague-Dawley rats that, when fed a high-fat diet, exhibit either an obesity-prone (DIO-P) or obesity-resistant (DIO-R) phenotype, to determine whether changes in gut epithelial function and microbiota are diet or obese associated. Food intake and body weight were monitored daily in rats maintained on either low-or high-fat diets. After 8 or 12 wk, tissue was removed to determine adiposity and gut epithelial function and to analyze the gut microbiota using PCR. DIO-P but not DIO-R rats exhibit an increase in toll-like receptor (TLR4) activation associated with ileal inflammation and a decrease in intestinal alkaline phosphatase, a luminal enzyme that detoxifies lipopolysaccharide (LPS). Intestinal permeability and plasma LPS were increased together with phosphorylation of myosin light chain and localization of occludin in the cytoplasm of epithelial cells. Measurement of bacterial 16S rRNA showed a decrease in total bacterial density and an increase in the relative proportion of Bacteroidales and Clostridiales orders in high-fat-fed rats regardless of phenotype; an increase in Enterobacteriales was seen in the microbiota of DIO-P rats only. Consumption of a high-fat diet induces changes in the gut microbiota, but it is the development of inflammation that is associated with the appearance of hyperphagia and an obese phenotype.