无毛基因敲除小鼠PPARγ-PGC1α-UCP1信号通路蛋白的表达及棕色脂肪组织能量代谢状态的变化  

Expression of PPARγ-PGC1α-UCP1 signaling pathway and energy metabolism of brown adipose tissue in hairless gene knockout mice

作　　者：何龙[1] 郭好雨 张超凡 杨紫薇 和娜娜 朱奎成 HE Long;GUO Haoyu;ZHANG Chaofan;YANG Ziwei;HE Nana;ZHU Kuicheng(Department of Anesthesiology,Perioperative Medicine,the First Affiliated Hospital,Zhengzhou University,Zhengzhou 450052;Platform of Laboratory Animal,Academy of Medical Sciences,Zhengzhou University,Zhengzhou 450052)

机构地区：[1]郑州大学第一附属医院麻醉与围术期医学部,郑州450052 [2]郑州大学医学科学院实验动物平台,郑州450052

出　　处：《郑州大学学报（医学版）》2023年第1期19-22,共4页Journal of Zhengzhou University(Medical Sciences)

基　　金：国家自然科学基金青年基金项目(82001189);河南省科技攻关计划(省部共建)项目(201911225)。

摘　　要：目的:探讨无毛(Hr)基因缺陷对小鼠能量代谢的影响及机制。方法:雄性Hr基因敲除(Hr^(-/-))小鼠和同窝野生型(Hr^(+/+))小鼠各10只,记录小鼠从出生后10周内的体重;于第10周,使用代谢监测系统对小鼠的耗氧量、产热量、活动量以及24 h进食量和饮水量进行监测,测量肛温,ELISA法检测血清游离三碘甲状腺原氨酸(fT3)浓度,HE染色观察棕色脂肪组织(BAT),Western blot法检测BAT中过氧化物酶体增殖物激活受体γ(PPARγ)、PPARγ共激活因子1α(PGC1α)、解偶联蛋白1(UCP1)蛋白的表达。结果:出生后第1周至第10周,两组小鼠体重差异无统计学意义(P>0.05)。第10周,两组小鼠血清fT3浓度和活动量差异无统计学意义(P>0.05);与Hr^(+/+)小鼠比较,Hr^(-/-)小鼠的肛温、24 h进食量和饮水量、耗氧量和产热量升高(P<0.05),BAT内较多小空泡脂滴和较少大空泡脂滴,BAT中PPARγ、PGC1α、UCP1蛋白表达增加(P<0.05)。结论:Hr基因缺陷可能通过激活PPARγ-PGC1α-UCP1信号通路,调节BAT能量代谢,从而使小鼠处于高能量代谢和高体温状态。Aim:To investigate the effects of hairless gene(Hr) deficiency on PPARγ-PGC1α-UCP1 signaling pathway and energy metabolism in brown adipose tissue(BAT) of mice.Methods:Male Hr knockout(Hr^(-/-)) and wild-type(Hr^(+/+)) mice, 10 in each group, were observed.Body weight within 10 weeks after birth was recorded.At the 10th week, activity, oxygen consumption(VO2),heat production, and food and water intake within 24 hours were monitored using a metabolic monitoring system, the anal temperature was measured, the serum free triiodothyronine(fT3) concentration was measured by ELISA,BAT in the scapular region was obtained to observe the morphological changes by HE staining, and peroxisome proliferator-activated receptor γ(PPARγ),PPARγ coactivator-1α(PGC1α),and uncoupling protein1(UCP1) protein expression in BAT was detected by Western blot.Results:From the 1st week to the 10th week, there was no significant difference in the body weight between the two group(P>0.05).There was no significant differences in the fT3 concentration or activity between the two groups(P>0.05);compared with those of the Hr^(+/+)mice, anal temperature, food and water intake within 24 hours, VO2and calorie production of Hr^(-/-)mice were higher(P<0.05),BAT had smaller lipid droplet vacuoles, and the expressions of PPARγ,PGC1α,and UCP1 in BAT of Hr^(-/-)mice increased(P<0.05).Conclusion:Hr gene deficiency may mediate higher energy metabolism and high body temperature of mice by activating the PPARγ-PGC1α-UCP1 signaling pathway and inducing BAT energy metabolism.

关 键 词：无毛基因 棕色脂肪组织 能量代谢 过氧化物酶体增殖物激活受体γ PPARγ共激活因子1α 解偶联蛋白-1 小鼠 

分 类 号：R339[医药卫生—人体生理学]