University of Chicago, Chicago, Illinois.
JPEN J Parenter Enteral Nutr. 2013 Nov;37(6):746-54. doi: 10.1177/0148607113486931. Epub 2013 May 2.
Growing evidence shows that dietary factors can dramatically alter the gut microbiome in ways that contribute to metabolic disturbance and progression of obesity. In this regard, mesenteric adipose tissue has been implicated in mediating these processes through the elaboration of proinflammatory adipokines. In this study, we examined the relationship of these events by determining the effects of dietary fat content and source on gut microbiota, as well as the effects on adipokine profiles of mesenteric and peripheral adipocytes.
Adult male C57Bl/6 mice were fed milk fat-based, lard-based (saturated fatty acid sources), or safflower oil (polyunsaturated fatty acid)-based high-fat diets for 4 weeks. Body mass and food consumption were measured. Stool 16S ribosomal RNA (rRNA) was isolated and analyzed via terminal restriction fragment length polymorphism as well as variable V3-4 sequence tags via next-generation sequencing. Mesenteric and gonadal adipose samples were analyzed for both lipogenic and inflammatory mediators via quantitative real-time polymerase chain reaction.
High-fat feedings caused more weight gain with concomitant increases in caloric consumption relative to low-fat diets. In addition, each of the high-fat diets induced dramatic and specific 16S rRNA phylogenic profiles that were associated with different inflammatory and lipogenic mediator profiles of mesenteric and gonadal fat depots.
Our findings support the notion that dietary fat composition can both reshape the gut microbiota and alter host adipose tissue inflammatory/lipogenic profiles. They also demonstrate the interdependency of dietary fat source, commensal gut microbiota, and inflammatory profile of mesenteric fat that can collectively affect the host metabolic state.
越来越多的证据表明，饮食因素可以显著改变肠道微生物群，从而导致代谢紊乱和肥胖的发展。在这方面，肠系膜脂肪组织通过产生促炎脂肪因子而被认为在介导这些过程中起作用。在这项研究中，我们通过确定饮食脂肪含量和来源对肠道微生物群的影响以及对肠系膜和外周脂肪细胞脂肪因子谱的影响来研究这些事件之间的关系。
成年雄性 C57Bl/6 小鼠喂食基于乳脂、猪油（饱和脂肪酸来源）或红花油（多不饱和脂肪酸）的高脂肪饮食 4 周。测量体重和食物摄入量。分离粪便 16S 核糖体 RNA（rRNA），并通过末端限制性片段长度多态性以及通过下一代测序的可变 V3-4 序列标签进行分析。通过定量实时聚合酶链反应分析肠系膜和性腺脂肪组织中的脂肪生成和炎症介质。
高脂肪喂养导致体重增加更多，同时热量消耗增加相对于低脂肪饮食。此外，每种高脂肪饮食都会引起剧烈和特定的 16S rRNA 系统发育图谱，这些图谱与肠系膜和性腺脂肪组织中不同的炎症和脂肪生成介质图谱相关。
我们的研究结果支持这样一种观点，即饮食脂肪成分既可以重塑肠道微生物群，又可以改变宿主脂肪组织的炎症/脂肪生成谱。它们还表明，饮食脂肪来源、共生肠道微生物群和肠系膜脂肪的炎症谱之间存在相互依存关系，它们可以共同影响宿主的代谢状态。
