Gong Li-Jing, Fu Peng-Yu, Zhu Rong-Xin, Wang Lei, Hu Yang
Chinese Academy of Sports and Health, Beijing Sport University, Beijing 100084, China.
Sport Science College, Beijing Sport University, Beijing 100084, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2018 Jan 8;34(1):88-92. doi: 10.12047/j.cjap.5507.2018.022.
This study intended to screen differentially expressed genes and pathways in Brown Adipose Tissue (BAT) of obese mice after the intervention of hypoxia by mRNA expression profile microarray, exploring the mechanism of hypoxia activated BAT.
Thirty C57BL/6J male mice were divided into the normal diet control group (N, =8), high-fat diet control group (OB, =8) and high-fat diet hypoxia group (H, =8). Group H was intervened by hypoxia exposure in the oxygen concentration of 11.2% of the normal oxygen and hypoxia for 8 h/d, 6 d/w of 4 weeks. Blood lipid and blood glucose were detected after intervention; RNA microarray scan and bioinformation analysis were done of BAT from scapula. Genes significantly ( ≤ 0.05) regulated more than 1.5 fold were chosen to do Gene Ontology and enrichment analysis by KOBAS 2.0, and confirmation of genes participating in key biological process (BP) and pathway was done by real time qPCR.
After intervention, the body weight and blood lipid and glucose levels in group H were significantly lower than those of group OB. Comparing with group N, 802 genes were significantly up-regulated and 1 175genes were down-regulated. The BP of these genes mainly concerned with glucose and lipid metabolic process and inflammatory reaction. Comparing with group OB, 297 genes were significantly up-regulated and 228 genes were down-regulated. These genes participated in glucose and lipid metabolic process, lipid transport, muscle system process and cardiovascular system development. The pathways of regulating BAT by hypoxia exposure mainly concentrated on the HIF-1, PI3K-AKT, FoxO and ErbB signaling pathways.
A series of genes and pathways in BAT could be adjusted by hypoxia exposure, so that hypoxia could improve the activity of BAT, promoting obese organism to lose weight.
本研究旨在通过mRNA表达谱芯片筛选肥胖小鼠棕色脂肪组织（BAT）在缺氧干预后的差异表达基因及通路，探讨缺氧激活BAT的机制。
将30只C57BL/6J雄性小鼠分为正常饮食对照组（N，n = 8）、高脂饮食对照组（OB，n = 8）和高脂饮食缺氧组（H，n = 8）。对H组进行缺氧暴露干预，在氧浓度为正常氧的11.2%的环境中，每天8小时，每周6天，共4周。干预后检测血脂和血糖；对肩胛下BAT进行RNA微阵列扫描和生物信息分析。选择差异倍数≥1.5且差异有统计学意义（P≤0.05）的基因，通过KOBAS 2.0进行基因本体论和富集分析，并通过实时定量PCR对参与关键生物学过程（BP）和通路的基因进行验证。
干预后，H组的体重、血脂和血糖水平均显著低于OB组。与N组相比，有802个基因显著上调，1175个基因下调。这些基因的BP主要涉及糖脂代谢过程和炎症反应。与OB组相比，有297个基因显著上调，228个基因下调。这些基因参与糖脂代谢过程、脂质转运、肌肉系统过程和心血管系统发育。缺氧暴露调节BAT的通路主要集中在HIF-1、PI3K-AKT、FoxO和ErbB信号通路。
缺氧暴露可调节BAT中的一系列基因和通路，从而提高BAT的活性，促进肥胖机体减重。
