脂肪组织在CYP1B1缺失保护小鼠营养性肥胖中的作用

Role of White Adipose Tissue in Protecting CYP1B1 Knock-out Mice from Obesity

目的:从脂肪组织脂肪代谢和相关内分泌功能方面探讨CYP1B1在成年小鼠营养性肥胖中的作用。方法:CYP1B1基因敲除和野生型雄性6周龄小鼠各16只,给予低、高脂饲料共6周。处理结束后分离脂肪组织,采用实时荧光定量PCR技术测定脂肪组织中相关因子表达水平,免疫印记检测葡萄糖转运蛋白4(GLUT4)表达。结果:与野生高脂组比较,基因敲除高脂组小鼠体重增量低;荧光定量PCR结果显示,敲除高脂组小鼠白介素-6(IL-6)、血管生成素2、脂肪酸结合蛋白2(AP2)等基因表达分别是野生高脂组的0.42,0.36,0.29倍,血管生成素1基因表达是野生高脂组的1.76倍。结论:CYP1B1基因缺失,可能通过对脂肪组织脂肪代谢、炎症状态、血管新生等综合影响,改善营养性肥胖及胰岛素抵抗。

Objective： To investigate the role of white adipose tissue（WAT） in protecting CYP1B1 knock-out mice from obesity.Methods： Sixteen male CYP1B1 knock-out adult mice and sixteen wild type mice（C57） were both randomly divided into low-fat-diet（LFD） and high-fat-diet（HFD） groups.The mice were scarified at the age of 12 weeks by decapitation;epididymal fat pad was collected for gene and protein expression.Results： High fat diet substaintially increased body weight gains and epididymal fat pad weight in WT mice other than KO group.IL-6,Angio2,GLUT4 expression in fat pad were upregulated by HFD and suppressed by CYP1B1 deletion,however,CYP1B1 raise Angio1 level in both LFD and HFD group.Conclusion： CYP1B1 deficiency regulates the expressions of critical factors in adipocyte metabolism,inflammation,angiogenesis and insulin signaling pathway,which may constitute a principle pathway that ameliorated obesity and the consequential insulin resistance.