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作 者:查成喜[1] 漆亚亚 柳渊洁[1] 邢福军[1] ZHA Cheng-xi;QI Ya-ya;LIU Yuan-jie;XING Fu-jun(Department of Clinical Laboratory, Gansu Provincial Hospital of TCM,Lanzhou 730050, Gansu Province, China)
机构地区:[1]甘肃省中医院检验科,甘肃兰州730050 [2]兰州大学第一医院生物转化医学实验中心,甘肃兰州730000
出 处:《中国生物制品学杂志》2019年第5期517-520,共4页Chinese Journal of Biologicals
基 金:兰州市科技计划项目(2014/1/12)
摘 要:目的探讨内脂素在糖尿病模型小鼠糖脂代谢中的作用。方法通过基因工程技术构建内脂素转基因和基因敲除小鼠,同时以野生小鼠作为对照,3组小鼠均以高脂高糖饮食饲养1个月后,于空腹12 h、进食30 min及1、2和3 h用血糖检测仪检测血糖水平;小鼠禁食10 h用生化分析仪检测甘油三酯、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇的水平;Western blot法检测小鼠体内内脂素表达水平;相应试剂盒检测小鼠体内胰岛素受体及胰岛素水平。结果除空腹12 h组外,进食30 min及1、2和3 h转基因组小鼠血糖水平明显低于基因敲除组和野生组(P <0. 05),野生组小鼠血糖水平显著低于基因敲除组(P <0. 01);转基因组小鼠甘油三酯、总胆固醇、高密度脂蛋白胆固醇水平显著低于基因敲除组(P <0. 05);基因敲除组小鼠内脂素表达水平明显低于转基因组和野生组(P <0. 001),转基因组小鼠明显高于野生组(P <0. 001);转基因小鼠胰岛素受体水平显著高于基因敲除小鼠和野生型小鼠(P <0. 01),野生型组明显高于基因敲除组(P <0. 05),3组间胰岛素水平差异无统计学意义(P> 0. 05)。结论内脂素通过与胰岛素非竞争性结合胰岛素受体而发挥降低糖尿病小鼠血糖作用,且在脂代谢中具有促进脂肪积累的功能。Objective To investigate the role of visfatin in glucose and lipid metabolism of diabetic mice. Methods Genetically engineered visfatin transgenic and gene knockout mouse models were established. The model mice were fed with a high-fat and high-sugar diet for one month,of which the blood glucose levels were determined by blood glucose analyzer 12 h after fasting and 30 min,1,2 and 3 h after food intake,serving wild mice as control. Triglyceride,total cholesterol,high density lipoprotein cholesterol and low density lipoprotein cholesterol levels were determined 10 h after fasting. The expression level of visfatin in vivo was determined by Western blot,while the insulin receptor and insulin levels by the corresponding kits. Results The blood glucose levels in transgenic mice 30 min,1,2 and 3 h after food intake were significantly lower than those in wild mice and in the mice with gene knockout(P < 0. 05). However,the blood glucose level of wild mice was significantly lower than that of mice with gene knockout(P < 0. 01). The triglyceride,total cholesterol and high density lipoprotein cholesterol levels of transgenic mice were significantly lower than those of mice with gene knockout(P < 0. 05). The expression level of visfatin was significantly lower in the mice with gene knockout than in transgenic and wild mice(P < 0. 001),and was significantly higher in transgenic mice than in wild mice(P < 0. 001). The insulin receptor level was significantly higher in transgenic mice than in the mice with gene knockout and in wild mice(P < 0. 01),and in wild mice than in the mice with gene knockout(P < 0. 05). However,no significant difference was observed in the insulin levels of mice in the three groups(P > 0. 05). Conclusion Visfatin decreased the blood glucose level of diabetic mice by non-competitive binding to insulin receptor with insulin,and promoted the fat accumulation in lipid metabolism.
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