肥胖和缺氧对小鼠原代脂肪细胞分泌TNFα的影响  

Effect of obesity and hypoxia on TNFα secretion by primary adipocytes in mice

作　　者：马晓芳[1] 童静凯 牛文彦[1] 

机构地区：[1]天津医科大学免疫学系,天津300070

出　　处：《天津医科大学学报》2014年第1期1-3,共3页Journal of Tianjin Medical University

基　　金：国家自然科学基金面上项目(81170740);国家自然科学基金委国际合作项目(81161120545);高等学校博士学科点专项基金(20121202110014)

摘　　要：目的:常氧和缺氧培养正常和肥胖小鼠的原代脂肪细胞,比较其分泌的肿瘤坏死因子α(TNFα)水平,探讨缺氧在脂肪组织慢性炎症中的作用。方法:高脂及普通饮食喂养4周龄C57BL/6雄性小鼠16周,测量体质量、葡萄糖耐量、胰岛素耐量;处死小鼠后取睾周脂肪组织,提取原代脂肪细胞,常氧或缺氧培养24 h后取上清,ELISA法测定培养基中TNFα的浓度。结果:高脂饮食喂养造成小鼠肥胖和胰岛素抵抗。常氧培养的肥胖小鼠脂肪细胞较正常小鼠的脂肪细胞分泌更多的TNFα;缺氧孵育比常氧孵育的正常小鼠脂肪细胞分泌更多的TNFα;但缺氧不进一步增加肥胖小鼠脂肪细胞分泌TNFα。结论:缺氧和肥胖均上调小鼠原代脂肪细胞TNFα的分泌,但缺氧不影响肥胖小鼠脂肪细胞分泌TNFα,提示肥胖小鼠脂肪细胞缺氧与其慢性炎症及胰岛素抵抗有关。Objective： To explore the effect of hypoxia on adipose tissue inflammation by culturing primary adipoeytes from lean and obese mice under normoxia or hypoxia condition and measuring the TNFa levels in the culture medium （conditioned dedium, CM）. Methods： 4- week old C57BL/6 male mice were fed with high fat diet （HFD） or chow diet （LFD） for 16 weeks, then body weight, intraperitoneal glucose tolerance test （ipGTT） and insulin tolerance test （ITT） were performed. The epididymal fat pads were taken and primary adipocytes were isolated and cultured under normoxic or hypoxic condition for 24 h. The levels of tumor necrosis factor-a （TNFa） in CMs were determined by ELISA. Results： HFD increased body weight and caused insulin resistance. Adipocytes in obese mice secreted higher level of TNFa than normal mice. Hypoxia treatment increased the level of TNFa secreted by adipocytes in normal mice. However, hypoxia did not affect TNFa secretion in obese mice. Conclusion： Both hypoxia and obese up-regulate TNFa secretion from murine primary adipocytes, but hypoxia does not further increase TNFa secretion from adipocytes of obese mice.

关 键 词：肥胖 脂肪细胞 缺氧 肿瘤坏死因子A 炎症 胰岛素抵抗 小鼠 

分 类 号：R398[医药卫生—基础医学]