Mabrok Hoda B, Ramadan Asmaa A, Hamed Ibrahim M, Mohamed Doha A
Nutrition and Food Science Department, Food Industries and Nutrition Institute, National Research Centre, Dokki, Cairo 12622, Egypt.
Brain Sci. 2024 Aug 12;14(8):807. doi: 10.3390/brainsci14080807.
Diet-induced obesity is a global phenomenon that affects the population worldwide with manifestations at both the phenotypic and genotypic levels. Cognitive function decline is a major global health challenge. The relation between obesity and cognitive function is a debatable issue. The main goal of the current research was to study the implications of obesity on cognitive function and gut microbiota diversity and its impact on plasma and brain metabolic parameters in rats. Obesity was induced in rats by feeding on a high-fat (HF) or a high-fat/high-sucrose (HFHS) diet. The results reveal that both the HF (0.683) and HFHS (0.688) diets were effective as obesity inducers, which was confirmed by a significant increase in the body mass index (BMI). Both diet groups showed dyslipidemia and elevation of oxidative stress, insulin resistance (IR), and inflammatory markers with alterations in liver and kidney functions. Obesity led to a reduction in cognitive function through a reduction in short-term memory by 23.8% and 30.7% in the rats fed HF and HFHS diets, respectively, and learning capacity and visuo-spatial memory reduced by 8.9 and 9.7 s in the rats fed an HF or HFHS diet, respectively. Bacteroidetes, Firmicutes, Proteobacteria, Fusobacteria, and Spirochaetes phyla were detected. The Firmicutes/Bacteroidetes ratio (F/B) significantly decreased in the HF group, while it increased in the HFHS group compared to the normal control. The two species, and , which are associated with IR, were drastically compromised by the high-fat/high-sucrose diet. Some species that have been linked to reduced inflammation showed a sharp decrease in the HFHS group, while , which is linked to carbohydrate metabolism, was highly enriched. In conclusion: Obesity led to cognitive impairment through changes in short-term and visuo-spatial memory. A metagenomic analysis revealed alterations in the abundance of some microbial taxa associated with obesity, inflammation, and insulin resistance in the HF and HFHS groups.
饮食诱导的肥胖是一种全球现象，影响着世界各地的人群，在表型和基因型水平上均有表现。认知功能下降是一项重大的全球健康挑战。肥胖与认知功能之间的关系是一个有争议的问题。当前研究的主要目标是研究肥胖对大鼠认知功能和肠道微生物群多样性的影响及其对血浆和脑代谢参数的作用。通过给大鼠喂食高脂肪（HF）或高脂肪/高蔗糖（HFHS）饮食来诱导肥胖。结果显示，HF（0.683）和HFHS（0.688）饮食作为肥胖诱导剂均有效，这通过体重指数（BMI）的显著增加得到证实。两个饮食组均出现血脂异常以及氧化应激、胰岛素抵抗（IR）和炎症标志物升高，同时伴有肝肾功能改变。肥胖导致认知功能下降，喂食HF和HFHS饮食的大鼠短期记忆分别降低了23.8%和30.7%，喂食HF或HFHS饮食的大鼠学习能力和视觉空间记忆分别降低了8.9秒和9.7秒。检测到拟杆菌门、厚壁菌门、变形菌门、梭杆菌门和螺旋体门。与正常对照组相比，HF组的厚壁菌门/拟杆菌门比例（F/B）显著降低，而HFHS组则升高。与IR相关的两种菌，[具体菌名1]和[具体菌名2]，受到高脂肪/高蔗糖饮食的严重影响。一些与炎症减轻相关的菌种在HFHS组中急剧减少，而与碳水化合物代谢相关的[具体菌名3]则高度富集。总之：肥胖通过短期和视觉空间记忆的改变导致认知障碍。宏基因组分析显示，HF组和HFHS组中一些与肥胖、炎症和胰岛素抵抗相关的微生物类群丰度发生了改变。
