摘要
目的氧化应激是引起胰岛素抵抗(insulin resistance,IR)的机制之一,而解偶联蛋白2(uncoupling protein 2,UCP2)具有抗氧化应激作用,但UCP2与IR之间关系尚不清楚。文中探讨UCP2基因表达与氧化应激及IR之间的关系。方法 8周龄SD大鼠16只,随机分为对照组和高脂组,每组8只,饲养12周。分别于第4、8及12周内眦静脉取血测定血清丙二醛(malonaldehyde,MDA)、超氧化物歧化酶(superoxide dismutase,SOD)及空腹胰岛素(fasting insulin,FINS)水平,并计算胰岛素抵抗(homeostasis model assessment of insulin resistance,HOMA-IR)指数。第12周处死大鼠,留取血液及肝、脂肪组织,检测血脂、血清脂联素(adiponectin,APN)及游离脂肪酸(free fatty acids,FFA),实时荧光定量PCR方法,比较2组大鼠肝及脂肪细胞中UCP2 mRNA表达水平。结果①第4周,2组大鼠血清MDA及SOD水平无显著差异,第8周高脂组大鼠血清MDA显著高于对照组,而SOD水平显著低于对照组(P<0.05),第12周时差异更显著。②第12周,高脂组大鼠的HOMA-IR显著高于对照组(P<0.05),而第4周及8周2组间HOMA-IR无显著差异。③实验结束时,高脂组大鼠的三酰甘油(triglycer-ide,TG)、FINS及FFA显著高于对照组,而APN显著低于对照组(P<0.05)。高脂组大鼠肝及脂肪细胞UCP2 mRNA表达分别比对照组增高77.4%和54.4%,其差异有统计学意义(P<0.05)。结论氧化应激可能是高脂诱导大鼠IR的始动因素,而UCP2 mRNA表达增加可能是应对氧化应激的一种代偿机制,在IR发生过程中起到保护作用。
Objective Oxidative stress is one of the mechanisms of insulin resistance（IR）,and uncoupling protein 2（UCP2） functions as an inhibitor of oxidative stress,but the relationship between UCP2 and IR remains unclear.Our aim is to study the relationships of the UCP2 expression with oxidative stress and IR in high-fat-fed rats.Methods Sixteen SD rats were equally randomized into a normal diet control（NC） and a high-fat（HF） diet group and fed for 12 weeks.Serum MDA,SOD and fasting insulin（FINS） were detected,and the HOMA-IR index calculated at 4,8 and 12 weeks.All the rats were killed at 12 weeks for the mea-surement of blood lipids,serum adiponectin（APN） and free fatty acids（FFA）,and real-time PCR was used to determine the expression of UCP2 in the liver and fat.Results At 8 and 12 weeks,MDA was remarkably higher while SOD significantly lower in the HF than in the NC group（P0.05）.At 12 weeks,HOMA-IR was markedly higher in the former than in the latter（P0.05）,but showed no significant difference between the two groups at 4 and 8 weeks.Compared with the NC group at the end of the experiment,the HF group exhibited significantly higher levels of triglyceride,FINS and FFA and a lower level of APN（P0.05）,as well as remarkably increased mRNA expression of UCP2 in the liver and fat（77.4% and 54.4%,P0.05）.Conclusion Oxidative stress may be an initial key event triggering HF-induced insulin resistance,while the increased expression of UCP2 may be a compensation mechanism for oxidative stress and play a protective role in the progression of insulin resistance.
出处
《医学研究生学报》
CAS
2011年第4期346-349,共4页
Journal of Medical Postgraduates
基金
江苏省自然科学基金(BK2008061)
南京市医学重点科技发展项目(ZKX05022)
关键词
氧化应激
胰岛素抵抗
解偶联蛋白2
Oxidative stress
Insulin resistance
Uncoupling protein 2
