The Transplantation of ω3 PUFA-Altered Gut Microbiota of fat-1 Mice to Wild-Type Littermates Prevents Obesity and Associated Metabolic Disorders
The Transplantation of ω3 PUFA-Altered Gut Microbiota of fat-1 Mice to Wild-Type Littermates Prevents Obesity and Associated Metabolic Disorders
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DOI：
10.2337/db17-1488
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发表时间：
2018-08-01
期刊：
影响因子：
7.7
通讯作者：
Bellenger, Jerome
中科院分区：
文献类型：
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作者：
Bidu, Celia;Escoula, Quentin;Bellenger, Jerome
改变肠道微生物组可能对宿主有益，最近被认为是控制肥胖的一种有前途的策略。在这里，我们研究了omega 3多不饱和脂肪酸（PUFA）介导的微生物群改变对小鼠代谢参数变化的相对贡献。比较了四组：雄性fat-1转基因小鼠（具有ω 3 PUFA的组成性产生）和雄性野生型（WT）同窝出生的小鼠，喂食致肥胖（高脂肪/高蔗糖[HFHS]）或对照饮食。与WT小鼠不同，HFHS喂养的fat-1小鼠可防止肥胖、葡萄糖耐受不良和肝脂肪变性。与WT小鼠不同，fat-1小鼠保持正常的屏障功能，导致代谢性内毒素血症显著降低。fat-1小鼠在盲肠中表现出更大的促生长多样性，从fat-1小鼠到WT小鼠的粪便微生物群移植能够逆转体重增加并使葡萄糖耐量和肠通透性正常化。我们得出结论，ω 3 PUFA介导的肠道微生物群的改变有助于预防fat-1小鼠的代谢综合征。它的发生独立的宿主组织中的PUFA含量的变化，并可能代表一个有前途的策略，以防止代谢疾病和保持精益表型。
Altering the gut microbiome may be beneficial to the host and recently arose as a promising strategy to manage obesity. Here, we investigated the relative contribution of omega 3 polyunsaturated fatty acid (PUFA)-mediated alterations in the microbiota to metabolic parameter changes in mice. Four groups were compared: male fat-1 transgenic mice (with constitutive production of omega 3 PUFAs) and male wild-type (WT) littermates fed an obesogenic (high fat/high sucrose [HFHS]) or a control diet. Unlike WT mice, HFHS-fed fat-1 mice were protected against obesity, glucose intolerance, and hepatic steatosis. Unlike WT mice, fat-1 mice maintained a normal barrier function, resulting in a significantly lower metabolic endotoxemia. The fat-1 mice displayed greater phylogenic diversity in the cecum, and fecal microbiota transplantation from fat-1 to WT mice was able to reverse weight gain and to normalize glucose tolerance and intestinal permeability. We concluded that the omega 3 PUFA-mediated alteration of gut microbiota contributed to the prevention of metabolic syndrome in fat-1 mice. It occurred independently of changes in the PUFA content of host tissues and may represent a promising strategy to prevent metabolic disease and preserve a lean phenotype.