Park Sang-Seo, Kim Tae-Woon, Kim Bo-Kyun, Kim Seong-Hyun, Park Jong-Suk, Shin Mal-Soon
Department of Physiology, College of Medicine, Kyung Hee University, Seoul, Korea.
Department of Human Health Care, Gyeongsang National University, Jinju, Korea.
J Exerc Rehabil. 2022 Jun 27;18(3):171-178. doi: 10.12965/jer.2244278.139. eCollection 2022 Jun.
The aim of this study was to investigate the effects of exercise and diet on mental status, insulin signaling pathway, serotonin synthesis, and microbiome in high-fat-induced obesity mice. Before the start of this experiment, obesity groups made obese mice by administering a high-fat diet containing 60% fat for 12 weeks. In the obesity with exercise group, after a high-fat diet for 12 weeks, exercise was performed with high-fat diet for 8 weeks. In the obesity with diet group, a high-fat diet for 12 weeks followed by a normal diet for 8 weeks. Depression and anxiety were determined by open field test and elevated plus maze test. Immunohistochemistry for tryptophan hydroxylase (TPH) in the dorsal raphe, western blot analysis for phosphorylated protein kinase B (p-ATK), total AKT (t-AKT), phosphorylated phosphoinositide 3-kinase (p-PI3K), and total PI3K (t-PI3K) in the hippocampus were performed. Analysis of microbiome was also conducted. Obesity-induced depression and anxiety status, suppressed ratio of p-AKT/t-AKT and p-PI3K/t-PI3K, and inhibited TPH synthesis. Exercise and diet improved depression and anxiety status, activated p-AKT/t-AKT and p-PI3K/t-PI3K, and increased TPH synthesis. Exercise and diet improved depression and anxiety status by increasing the insulin signaling pathway and promoting serotonin production. These effects of exercise and diet were almost similar. In addition, exercise and diet regulated the composition of gut microbiota.
本研究旨在探讨运动和饮食对高脂诱导肥胖小鼠的精神状态、胰岛素信号通路、血清素合成及微生物群的影响。在本实验开始前,肥胖组通过给予含60%脂肪的高脂饮食12周使小鼠肥胖。在运动加肥胖组中,高脂饮食12周后,继续高脂饮食并运动8周。在饮食加肥胖组中,高脂饮食12周后,改为正常饮食8周。通过旷场试验和高架十字迷宫试验测定抑郁和焦虑情况。对中缝背核中的色氨酸羟化酶(TPH)进行免疫组织化学分析,对海马体中的磷酸化蛋白激酶B(p-ATK)、总AKT(t-AKT)、磷酸化磷脂酰肌醇3激酶(p-PI3K)和总PI3K(t-PI3K)进行蛋白质免疫印迹分析。同时进行微生物群分析。肥胖诱导抑郁和焦虑状态,抑制p-AKT/t-AKT和p-PI3K/t-PI3K的比例,并抑制TPH合成。运动和饮食改善了抑郁和焦虑状态,激活了p-AKT/t-AKT和p-PI3K/t-PI3K,并增加了TPH合成。运动和饮食通过增加胰岛素信号通路和促进血清素产生改善了抑郁和焦虑状态。运动和饮食的这些作用几乎相似。此外,运动和饮食调节了肠道微生物群的组成。