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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 CYP1B1 in nutritional obesity in adult mice from the aspects of fat metabolism and related endocrine function in adipose tissue. METHODS: Sixteen CYP1B1 knockout and wild-type male 6-week-old mice were given low and high-fat diet for 6 weeks. Adipose tissue was isolated after treatment, and the expression of related factors in adipose tissue was detected by real-time fluorescence quantitative PCR. The expression of GLUT4 was detected by immunoblotting. Results: Compared with the wild hyperlipidemia group, the gene knockout hyperlipidemia group had a low body weight gain. Fluorescent quantitative PCR results showed that the knockdown of IL-6, angiopoietin 2, fatty acid The gene expression of binding protein 2 (AP2) was 0.42, 0.36 and 0.29 times higher than wild hyperlipidemia group, and the expression of angiopoietin 1 gene was 1.76 times higher than wild hyperlipemia group. Conclusion: The deletion of CYP1B1 gene may improve nutritional obesity and insulin resistance through the combined effects of fat metabolism, inflammatory status and angiogenesis.