Université de Bourgogne Franche-Comté, UFR Sciences de la Vie, de la Terre et de l'Environnement, Lipides Nutrition Cancer UMR UMR1231, 6 Boulevard Gabriel, 21000, Dijon, France; INSERM, Lipides Nutrition Cancer UMR1231, 21000, Dijon, France; LipSTIC LabEx, Fondation de Coopération Scientifique Bourgogne-Franche Comté, 21000, Dijon, France.
Université de Bourgogne Franche-Comté, UFR Sciences de la Vie, de la Terre et de l'Environnement, Lipides Nutrition Cancer UMR UMR1231, 6 Boulevard Gabriel, 21000, Dijon, France; INSERM, Lipides Nutrition Cancer UMR1231, 21000, Dijon, France; LipSTIC LabEx, Fondation de Coopération Scientifique Bourgogne-Franche Comté, 21000, Dijon, France.
Biochimie. 2019 Apr;159:66-71. doi: 10.1016/j.biochi.2019.01.017. Epub 2019 Jan 25.
Obesity is now widely recognized to be associated with low-grade systemic inflammation. It has been shown that high-fat feeding modulates gut microbiota which strongly increased intestinal permeability leading to lipopolysaccharide absorption causing metabolic endotoxemia that triggers inflammation and metabolic disorders. N-3 polyunsaturated fatty acids (PUFAs) have been shown associated with anti-obesity properties, but results still remain heterogeneous and very few studies underlined the metabolic pathways involved. Thus, the use of Fat-1 transgenic mice allows to better understanding whether endogenous n-3 PUFAs enrichment contributes to obesity and associated metabolic disorders prevention. It specially evidence that such effects occur through modulations of gut microbiota and intestinal permeability. Then, by remodeling gut microbiota, endogenous n-3 PUFAs improve HF/HS-diet induced features of the metabolic syndrome which in turn affects host metabolism. Thus, increasing anti-obesogenic microbial species in the gut microbiota population (i.e Akkermansia) by appropriate n-3 PUFAs may represent a promising strategy to control or prevent metabolic diseases.
肥胖症现在被广泛认为与低度全身炎症有关。研究表明,高脂肪喂养会调节肠道微生物群,这会强烈增加肠道通透性,导致内毒素吸收,引发炎症和代谢紊乱。n-3 多不饱和脂肪酸(PUFAs)与抗肥胖特性有关,但结果仍然存在异质性,很少有研究强调涉及的代谢途径。因此,使用 Fat-1 转基因小鼠可以更好地了解内源性 n-3 PUFAs 的富集是否有助于预防肥胖症和相关代谢紊乱。特别有证据表明,这些作用是通过调节肠道微生物群和肠道通透性来实现的。然后,通过重塑肠道微生物群,内源性 n-3 PUFAs 改善了 HF/HS 饮食诱导的代谢综合征特征,进而影响宿主代谢。因此,通过适当的 n-3 PUFAs 增加肠道微生物群中抗肥胖微生物的种类(即 Akkermansia)可能是控制或预防代谢性疾病的一种有前途的策略。