罗格列酮干预糖尿病大鼠脂肪组织 CMKLR1及Chemerin基因表达

摘要

Objective:To investigate the expression of CMKLR1 and Chemerin mRNA in subcutaneous and visceral adipose tissue of rats and discuss the intervention of Chemerin-CMKLR1 to involve in the pathogenesis of obesity, insulin resistance and type 2 diabetes. Methods:Thirty male rats of 4 weeks were selected. Twenty rats were proved with diabetes through experimental methods after 30 weeks. Models were separated into rosiglitazone group and diabetes group with ten rats in each group. Experiment dates were detected. The mRNA levels of CMKLR1 and Chemerin in adipose tissue were detected by real-time PCR. Results:Experiments dates were improved after the intervention of rosiglitazone. The mRNA levels of CMKLR1 in visceral adipose tissue of rats in rosiglitazone group were lower than those in diabetes group (P<0.01).The mRNA levels of Chemerin of subcutaneous and visceral adipose tissue of rats in rosiglitazone group were lower than those in diabetes group (P<0.01). Maximum diameter in visceral adipocyte in rosiglitazone group decreased compared with that in diabetes group (P<0.01). Maximum diameter was no difference in subcutaneous tissue between two groups (P>0.05). Conclusion:The intervention of the expression of CMKLR1 and Chemerin mRNA become new treatment target of obesity and insulin resistance and type 2 diabetes by rosiglitazone.%目的：通过检测罗格列酮干预后CMKLR1及Chemerin在自发性2型糖尿病大鼠脂肪组织中表达水平，探讨Chemerin-CMKLR1通路在肥胖、胰岛素抵抗及2型糖尿病发病机制中的作用。方法：4周龄大鼠30只，经相关实验至30周证实造模成功2型糖尿病大鼠20只，再随机分为罗格列酮干预组和模型组各10只，进行相关实验室指标检测，以实时荧光定量法检测脂肪组织CMKLR1及Chemerin基因的表达水平。结果：罗格列酮干预后大鼠各实验室指标明显改善，干预组大鼠网膜组织CMKLR1的表达明显低于模型组（P<0.01），干预后网膜及皮下脂肪组织中Chemerin的表达明显低于模型组（P<0.01）。罗格列酮干预后网膜脂肪细胞平均最大直径明显缩小（P<0.01），而皮下脂肪细胞平均最大直径无明显变化（P>0.05）。结论：Chemerin-CMKLR1通路成为治疗肥胖、胰岛素抵抗和2型糖尿病的新靶点。