School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China; Department of nutrition, Beijing Daxing District People's Hospital, Beijing, China.
School of Public Health, Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, China.
J Nutr Biochem. 2022 May;103:108959. doi: 10.1016/j.jnutbio.2022.108959. Epub 2022 Feb 11.
High-fat diets are linked to obesity, contributing to the alterations in inflammatory signaling pathways, which is associated with cognitive function. We aim to investigate the mechanisms by which various different types of dietary fatty acids affecting cognitive function in obese mice through the gut/brain axis-inflammatory signaling pathway. 8-week-old male C57BL/6 mice were fed with basal diet (control group), lard high-fat diet (containing long-chain saturated fatty acid (LCSFA group)), coconut oil high-fat diet (containing medium-chain saturated fatty acid (MCSFA group)), linseed oil high-fat diet (containing n-3 polyunsaturated fatty acid (n-3 PUFA group)), soybean oil high-fat diet (containing n-6 polyunsaturated fatty acid (n-6 PUFA group)), olive oil high-fat diet (containing monounsaturated fatty acid (MUFA group)) and 8% hydrogenated soybean oil high-fat diet (containing trans fatty acid (TFA group)) respectively for 16 weeks. Our results revealed that the mean escape latency was significantly prolonged in LCSFA group, and the latency to cross the platform location of n-6 PUFA and TFA groups were increased significantly. The differences of inflammatory markers and toll-like receptor-myeloid differentiation factor-88-nuclear factor kappa-B (TLR-MyD88-NF-κB) inflammatory signaling pathway expressions among all groups reached statistical significances. Compared to basal diet, high-fat diets enriched in LCSFA, MCSFA, n-6 PUFA, MUFA, and TFA might exert detrimental effects on cognitive function in obese mice via regulating the inflammatory markers and inflammatory signaling pathway in brain and intestine. High-fat diet enriched in n-3 PUFA might exhibit different effect on modulating inflammatory responses in different tissues and might benefit to cognitive function.
高脂肪饮食与肥胖有关，导致炎症信号通路改变，与认知功能有关。我们旨在通过肠道/大脑轴-炎症信号通路研究各种不同类型的膳食脂肪酸通过何种机制影响肥胖小鼠的认知功能。8 周龄雄性 C57BL/6 小鼠分别用基础饮食（对照组）、猪油高脂肪饮食（含长链饱和脂肪酸（LCSFA 组））、椰子油高脂肪饮食（含中链饱和脂肪酸（MCSFA 组））、亚麻籽油高脂肪饮食（含 n-3 多不饱和脂肪酸（n-3 PUFA 组））、大豆油高脂肪饮食（含 n-6 多不饱和脂肪酸（n-6 PUFA 组））、橄榄油高脂肪饮食（含单不饱和脂肪酸（MUFA 组））和 8%氢化大豆油高脂肪饮食（含反式脂肪酸（TFA 组））喂养 16 周。结果显示，LCSFA 组的平均逃避潜伏期明显延长，n-6 PUFA 和 TFA 组的穿越平台位置潜伏期明显增加。各组炎症标志物和 Toll 样受体-髓样分化因子-88-核因子 kappa-B（TLR-MyD88-NF-κB）炎症信号通路表达的差异均有统计学意义。与基础饮食相比，富含 LCSFA、MCSFA、n-6 PUFA、MUFA 和 TFA 的高脂肪饮食可能通过调节大脑和肠道中的炎症标志物和炎症信号通路对肥胖小鼠的认知功能产生不利影响。富含 n-3 PUFA 的高脂肪饮食可能对调节不同组织中的炎症反应产生不同的影响，并可能有益于认知功能。
