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.

现在，肥胖被认为与低度全身性炎症有关。已经表明，高脂喂养可调节肠道微生物群，从而极大地增加肠道通透性，导致脂多糖吸收，引起代谢性内毒素血症，从而触发炎症和代谢性疾病。N-3多不饱和脂肪酸（PUFA）已显示与抗肥胖特性相关，但结果仍不统一，很少有研究强调相关的代谢途径。因此，使用Fat-1转基因小鼠可以更好地了解内源性n-3 PUFA的富集是否有助于肥胖症和相关代谢紊乱的预防。它特别证明了这种作用是通过调节肠道菌群和肠道通透性而发生的。然后，通过重塑肠道菌群，内源性n-3 PUFA可改善HF / HS饮食诱导的代谢综合征特征，进而影响宿主代谢。因此，肠道菌群中抗肥胖药的微生物种类不断增加（即Akkermansia）通过适当的n-3多不饱和脂肪酸可以代表有希望的策略来控制或预防代谢性疾病。