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作 者:胡燕荣 高莉[2] 杨海[2] 康永安[2] 周玲[2] 李南方[2]
机构地区:[1]新疆维吾尔自治区人民医院博士后工作站中国医学科学院北京协和医学院基础医学院博士后流动站,乌鲁木齐830001 [2]新疆维吾尔自治区人民医院高血压中心新疆高血压研究所
出 处:《中华生物医学工程杂志》2012年第6期441-444,共4页Chinese Journal of Biomedical Engineering
基 金:国家自然科学基金(81160109)
摘 要:目的研究饮食诱导的肥胖大鼠模型下丘脑、肝、胰等组织器官中G蛋白耦联的内向整流型K离子通道蛋白4(GIRK4)的表达。方法30只SD大鼠按随机数字表分两组,肥胖大鼠组(20只,高脂高糖饮食构建肥胖大鼠模型)和正常对照组(10只,正常饮食)。建模成功处死两组大鼠后分离下丘脑、肝、胰等组织器官,提取蛋白,Western免疫印迹检测GIRK4表达。对肥胖大鼠组与正常对照组大鼠体质量、体长、脂肪系数等指标进行分析比较。结果肥胖大鼠组大鼠体长、体质量、脂肪系数显著高于正常对照组雌:(22.00±0.71)比(20.80±-0.45)cm,,(289.10±29.06)比(239.60±10.08)g,(3.47±1.54)比(1.14±0.56);雄:(26.32±0.87)比(24.80±0.84)cm,(432.00±28.14)比(352.00±37.37)g,(3.20±0.56)比(1.11±0.27);均P〈0.05],但下丘脑、肝、胰脏的GIRK4表达却显著低于正常对照组(P〈0.05)。结论大鼠下丘脑、肝脏、胰脏较高表达的GIRK4可能与脂肪代谢、饮食诱导型肥胖的发生有关。Objective To investigate GIRK4 expression in hypothalamus, liver and pancreas of diet induced obesity rat model. Methods Thirty SD rats were randomly assigned to obesitygroup (n=20) as fed by high-fat and high-sugar diet for establishment of obesity model and normal control group (n=10) as fed by normal diet. The rats were sacrificed followed by separation of organs (i.e. hypothalamus, liver and pancreas). Protein of above organs was extracted for detection of GIRK4 expression via Western immunoblotting. The weight, length and fat coefficient were compared. Results Obese rats yielded markedly higher weight[female:(289.10±29.06) vs (239.60±10.08)g, male:(432.00±28.14) vs (352.00±37.37)g], length[female:(22.0(O.71 ) vs (20.80±0.45) cm, male:(26.32±0.87) vs (24.80±0.84)cm] and fat coefficient[female:(3.47±l.54) vs (1.14i-0.56), male:(3.20± 0.56) vs ( 1.11±20.27 ) ] yet significantly suppressed GIRK4 expression in hypothalamus, liver and pancreas than normal controls (all P〈0.05). Conclusion The up-regulation of GIRK4 expression in hypothalamus, liver and pancreas may be related to fat metabolism and obesity induced by diet.
关 键 词:疾病模型 动物 G蛋白耦联的内向整流型K离子通道蛋白4 肥胖症
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