缺氧(环境)
微阵列
生物
内分泌学
基因
褐色脂肪组织
脂肪组织
微阵列分析技术
内科学
基因表达
脂质代谢
生物化学
氧气
医学
化学
有机化学
作者
Lijing Gong,Pengyu Fu,Rongxin Zhu,Lei Wang,Yang Hu
出处
期刊:PubMed
日期:2018-01-08
卷期号:34 (1): 88-92
被引量:1
标识
DOI:10.12047/j.cjap.5507.2018.022
摘要
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, n=8), high-fat diet control group (OB, n=8) and high-fat diet hypoxia group (H, n=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 (P ≤ 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.
科研通智能强力驱动
Strongly Powered by AbleSci AI