Fang Jing, Wang Fengyuan, Song Hetao, Wang Zhengyi, Zuo Zhicai, Cui Hengmin, Jia Yiping, Deng Junliang, Yu Shumin, Hu Yanchun, Shen Liuhong, Ma Xiaoping, Ren Zhihua, Gou Liping
College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, Sichuan 611130, PR China.
Sichuan Center for Animal Disease Control and Prevention, Chengdu, Sichuan 610041, PR China.
Aging (Albany NY). 2018 Nov 6;10(11):3161-3172. doi: 10.18632/aging.101623.
To investigate the different effects of acute pulmonary infection induced by () on lipid metabolism between diet-induced obesity (DIO, fed with high-fat diet) mice and lean mice. A total of 180 ICR mice were selected to be challenged intranasally with phosphate-buffered saline or 10 CFUs/mL of , and the body character indexes, biochemical indexes and expressions of genes and proteins involved in lipid metabolism were examined pre- and post-infection. Results revealed that, before infection, DIO mice had significantly higher body weight, adipose and liver indexes, free fatty acid and triglyceride contents than lean mice. After infection, increased free fatty acid and triglyceride contents, increased expressions of resistin, SREBP-1c, ACC1, FAS and SCD-1, and declined PPARα, CPT-1α expressions and AMPKα phosphorylation were detected in the infected group, while the change rates were more serious in the lean mice than the DIO mice. The above-mentioned findings verified that, after being infected with , hepatic lipid metabolism disorder was aggravated by activating SREBP-1c related lipid synthesis pathway and inhibiting PPARα related fatty acid oxidation pathway. However, infection-induced lipid metabolic disorders was slighter in the DIO mice than the lean mice through AMPKα pathway.
为研究()诱导的急性肺部感染对饮食诱导肥胖(DIO,喂食高脂饮食)小鼠和瘦小鼠脂质代谢的不同影响。总共选择180只ICR小鼠经鼻用磷酸盐缓冲盐水或10 CFUs/mL的()进行攻击,并在感染前后检测身体特征指标、生化指标以及参与脂质代谢的基因和蛋白质表达。结果显示,感染前,DIO小鼠的体重、脂肪和肝脏指数、游离脂肪酸和甘油三酯含量显著高于瘦小鼠。感染后,感染组检测到游离脂肪酸和甘油三酯含量增加、抵抗素、SREBP-1c、ACC1、FAS和SCD-1表达增加,PPARα、CPT-1α表达和AMPKα磷酸化下降,而瘦小鼠的变化率比DIO小鼠更严重。上述结果证实,感染()后,通过激活SREBP-1c相关脂质合成途径和抑制PPARα相关脂肪酸氧化途径,肝脏脂质代谢紊乱加剧。然而,通过AMPKα途径,感染诱导的脂质代谢紊乱在DIO小鼠中比瘦小鼠更轻微。