摘要
目的:使用高脂饮食诱导(high fat diet-induced,HFD)的肥胖小鼠模型,研究过氧化物酶体增殖物激活受体γ(perox-isome proliferator-activated receptorγ,PPARγ)激动剂匹格列酮(pioglitazone,PGZ)对肥胖小鼠棕色脂肪组织功能的影响,及可能的作用机制。方法:建立HFD肥胖小鼠模型(n=30);肥胖小鼠随机分为PGZ灌胃组和对照组(每组15只),PGZ 10 mg/(kg.d)灌胃1个月,对照组使用等量生理盐水灌胃。检测灌胃组及对照组小鼠的体重、口服葡萄糖耐量(OGTT)、血胰岛素含量;使用RT-PCR检测小鼠棕色脂肪组织特异性基因表达;使用Western blot检测小鼠棕色脂肪组织UCP-1蛋白的表达量。结果:PGZ灌胃的肥胖小鼠棕色脂肪功能相关基因和蛋白表达提高;PGZ灌胃组小鼠体重、血胰岛素含量和口服葡萄糖耐量改善。结论:PGZ通过调节棕色脂肪功能基因表达提高棕色脂肪功能,可能是PGZ改善胰岛素抵抗和机体代谢的重要原因。
Objective：To explore the mechanism of pioglitazone（PGZ）on brown adipose tissue（BAT）function in insulin resistance and type 2 diabetes mellitus,by using high fat diet-induced obesity（HFD）mouse.Methods：The C57BL/6J mice were randomly divided into the normal diet group and high-fat diet（HFD）group.After 20 weeks,the HFD group mice were randomly divided into obese control group and PGZ treatment group.They were orally administered placebo and PGZ[10 mg/（kg·d）]respectively for one month.The levels of body weight,serum insulin and oral glucose tolerance were measured by Biochemistry technology;The effect of pioglitazone on brown adipose tissue（BAT）was assessed by real-time quantitative PCR and Western-blot.Results：The bodyweight,serum insulin levels increased（P 〈 0.05）and oral glucose tolerance decreased in HFD group.Comparing to obese controls,serum insulin,glucose levels significantly decreased（P 〈 0.05）,and oral glucose tolerance increased in PGZ treatment group;The expressions of proteins and mRNA relative to BAT function increased in PGZ treatment group.Conclusion：PGZ can enhance the function of BAT by regulating BAT relative gene and protein expressions,and may be the important reason of improving insulin resistance and metabolism in HFD mouse.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2011年第5期689-693,共5页
Journal of Nanjing Medical University(Natural Sciences)
基金
国家自然科学基金青年基金项目(30900504)
