肥胖大鼠骨骼肌AMPK表达及其与糖脂代谢的关系  被引量:10

The expression of AMPK in high-fat-fed rats′ muscles and the role AMPK plays on the metabolism of lipid and glucose

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作  者:程媛[1] 王佑民[1] 丁晓洁[1] 

机构地区:[1]安徽医科大学内分泌与代谢病研究所,合肥230022

出  处:《安徽医科大学学报》2010年第2期180-183,共4页Acta Universitatis Medicinalis Anhui

基  金:安徽省自然科学基金(编号:070413080);安徽省教育厅自然科学研究项目(编号:2006KJ089A)

摘  要:目的探讨肥胖大鼠骨骼肌组织腺苷酸活化蛋白激酶(AMPK)的表达及其对糖脂代谢的影响。方法将28只6周龄雄性SD大鼠随机分为普通饮食组(NC组,15只)和高脂饮食组(HF组,13只),分别测体重(BW)、血清游离脂肪酸(FFA)、甘油三脂(TG)、总胆固醇(TCH)、空腹血糖(FPG)、空腹胰岛素(FINS)等指标。采用免疫印迹法测定各组大鼠骨骼肌中AMPK和磷酸化AMPK(p-AMPK)的水平。以p-AMPK/AMPK代表AMPK的活性。结果与NC组大鼠相比,HF组大鼠的BW、FFA、TG、FPG、FINS均明显升高(P<0.05),骨骼肌中AMPK表达降低,但差异无统计学意义(P>0.05),p-AMPK表达及AMPK活性(p-AMPK/AMPK)降低显著(均P<0.05)。骨骼肌组织p-AMPK表达水平与FPG、FFA呈负相关(P<0.05),AMPK活性与FPG、FFA、TG呈负相关(P<0.05),与FINS无相关性。结论高脂饮食诱导大鼠营养性肥胖,降低AMPK的活性,从而导致TG和TCH的合成增加,血糖升高,脂质在外周组织沉积增加。Objective To investigate the expression of AMP-activated protein kinase (AMPK) in high-fat-fed rats′muscles.To explore the mechanism of AMPK on the metabolism of lipid and glucose.Methods 28 male SD rats were randomly divided into two groups:15 were fed with normal control diet as NC group;13 were fed with a high-fat diet as HF group.Body weight(BW),free fatty acids(FFA),triglyceride(TG),total cholesterol(TCH),fasting plasma glucose(FPG) and fasting insulin(FINS) were measured.The protein levels of AMPK and p-AMPK in the muscles of all the rats were analyzed with Western blot.Results The BW,FFA,TG,FPG and FINS in HF group were significantly higher than those in NC group.The expression of AMPK in the muscles of HF group was lower than that in NC group,but no significant difference.However,compared with NC group,HF group had a lower expression of p-AMPK in the muscles(P〈0.05).The activity of AMPK negatively regulated FPG,FFA andTG and had no significant relation with FINS.Conclusions High-fat nutrition diet can induce obesity in rats,reducing the activity of AMPK,so promote the synthesis of TG and TCH,elevate blood glucose,increase lipid deposition in peripheral tissue.

关 键 词:环AMP依赖性蛋白激酶类 肥胖症 

分 类 号:R345.8[医药卫生—基础医学] R151.1

 

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