Calbinotox (UR7488), Université de Lorraine, 54000 Nancy, France.
INRAE, Université Paris-Saclay, AgroParisTech, UMR 1319 Micalis Institute, 78352 Jouy-en-Josas, France.
Nutrients. 2022 Dec 15;14(24):5338. doi: 10.3390/nu14245338.
Although arachidonic acid (ARA) is the precursor of the majority of eicosanoids, its influence as a food component on health is not well known. Therefore, we investigated its impact on the gut microbiota and gut-brain axis. Groups of male BALB/c mice were fed either a standard diet containing 5% lipids (Std-ARA) or 15%-lipid diets without ARA (HL-ARA) or with 1% ARA (HL + ARA) for 9 weeks. Fatty acid profiles of all three diets were the same. The HL-ARA diet favored the growth of contrary to the HL + ARA diet that favored the pro-inflammatory genus in fecal microbiota. Dietary ARA intake induced 4- and 15-fold colic overexpression of the pro-inflammatory markers IL-1β and CD40, respectively, without affecting those of TNFα and adiponectin. In the brain, dietary ARA intake led to moderate overexpression of GFAP in the hippocampus and cortex. Both the hyperlipidic diets reduced IL-6 and IL-12 in the brain. For the first time, it was shown that dietary ARA altered the gut microbiota, led to low-grade colic inflammation, and induced astrogliosis in the brain. Further work is necessary to determine the involved mechanisms.
尽管花生四烯酸(ARA)是大多数类二十烷酸的前体,但它作为食物成分对健康的影响尚不清楚。因此,我们研究了它对肠道微生物群和肠脑轴的影响。将雄性 BALB/c 小鼠分为三组,分别用含有 5%脂质的标准饮食(Std-ARA)、不含 ARA 的 15%脂质饮食(HL-ARA)或含 1%ARA 的 15%脂质饮食(HL + ARA)喂养 9 周。三种饮食的脂肪酸谱相同。HL-ARA 饮食促进了肠道微生物群中促炎属的生长,而 HL + ARA 饮食则相反。饮食中 ARA 的摄入分别诱导了促炎标志物 IL-1β 和 CD40 的 4 倍和 15 倍的过度表达,而不影响 TNFα 和脂联素的表达。在大脑中,饮食中 ARA 的摄入导致海马体和皮质中 GFAP 的适度过度表达。两种高脂饮食均降低了大脑中的 IL-6 和 IL-12。这是首次表明饮食 ARA 改变了肠道微生物群,导致轻度结肠炎症,并在大脑中诱导了星形胶质细胞增生。需要进一步的工作来确定涉及的机制。