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机构地区:[1]武汉大学人民医院内分泌科,武汉430060 [2]荆门市第一人民医院神经内科,荆门448000
出 处:《营养学报》2005年第4期288-291,共4页Acta Nutrimenta Sinica
基 金:湖北省自然科学基金资助(No.2003ABA182)
摘 要:目的:在高脂饮食诱导胰岛素抵抗的基础上,观察低脂膳食对胰岛素抵抗大鼠脂肪组织中蛋白激酶B(proteinkinaseB,PKB)表达的影响。方法:雄性Wistar大鼠30只,随机分为正常对照组(controlgroup,C)10只,给予低脂饲料;模型组(modelgroup,M)20只,给予高脂饲料。喂养4w后,又随机分为2组:高脂喂养组(highfatdiet,HF),继续高脂饮食;低脂喂养组(lowfatdietedgroup,LF),给予低脂饮食。干预6w后,蛋白印迹法检测大鼠脂肪组织中胰岛素刺激PKB的蛋白表达含量。结果:1.高脂M组的空腹血糖(FBG)、胰岛素(FINS)、甘油三酯(TG)、胆固醇(TC)及胰岛素抵抗指数(homeostasismodelassessment-insulinresistanceindex,HOMA-IR)明显升高,胰岛素敏感指数(insulinresistanceindex,ISI)显著下降,出现了胰岛素抵抗。2.低脂膳食干预6w,LF组的FBG、TG、TC及HOMA-IR下降,ISI显著升高。3.长期高脂膳食,HF组大鼠脂肪组织中PKB的表达明显减少,较C组下降了23.5%。低脂饮食6w后,LF组大鼠PKB蛋白表达明显升高,较HF组增加了16.1%。结论:低脂膳食纠正糖脂代谢紊乱,改善胰岛素抵抗,可能与增加脂肪组织中PKB蛋白表达有关。Objective: To study the effect of low fat diet on expression of protein kinase B (PKB) in adipose tissue of rats with insulin resistance. Method: Thirty male Wistar rats were randomly divided into control group ( C, n=10), given low fat diet; model group (M, n=20), given high fat diet. After 4 w, group M was randomly divided into 2 subgroups accepting diet intervention of 6 w. (1) High fat group (HF) was continually given high fat diet; (2) Low fat group (LF) accepted low fat diet. The expression of PKB stimulated by insulin in adipose tissue was determined with Western blotting at the end of the experiment. Results: (1) Group M showed hyperglycemia, hyperinsulinism, hypertriglyceride, hypercholesterolemia and elevated HOMA insulin resistance index (HOMA-IR) while the insulin sensitivity index (ISI) was obviously reduced compared to group C, indicating that the insulin resistant model was induced ; (2) Low fat diet treatment decreased FBG, TG, TC, which were accompanied by lower HOMA-IR and elevated ISI; (3) Because of long term high fat diet. exoression of PKB in adioose tissue of grouo HF decreased bv 23.5% ( P 〈 0.01 ) compared with group C. There was an increase of 16.1% (P 〈 0.01 ) in PKB expression of group LF compared to group HF. Conclusion: Low fat diet can significantly elevate expression of PKB and ameliorate the state of insulin resistance.
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