本文選題：肥胖 + 運動��； 參考：《北京體育大學》2012年博士論文

【摘要】：目的： 研究運動和EGCG、肉堿對單純性肥胖大鼠減肥和脂代謝及基因表達的作用,并探討單純性肥胖發(fā)生的分子學機制。 方法： 建立肥胖大鼠模型。研究8周高脂飲食對其體重、內臟脂肪系數(shù)、血清TG、TC HDL濃度、組織TG、肝臟PPARα、PGC-1α、AMPKα2、CPT1、MCAD表達水平的影響,然后隨機選取肥胖造模成功大鼠30只進行減肥干預實驗,將其分為肥胖對照組(F),運動組(S),運動+EGCG組(S+E),運動+肉堿組(S+L),運動+EGCG+肉堿干預組(S+E+L),除F組外,其他四組大鼠進行低強度有氧跑臺訓練。實驗結束后測試各組大鼠的體重、內臟脂肪系數(shù)、血清TG、T、HDL濃度、組織TG水平、肝臟PPARα、PGC-1α、AMPKα2、CPT1、MCAD的基因及蛋白水平。 結果： 1.F組血清TG、TC高于正常對照組(C),HDL低于C組(P0.05)；肝臟TG較C組高(P0.05); PPARαmRNA及蛋白、PGC-1αmRNA、AMPK a2蛋白顯著低于C組.(P0.05)； 2.與F組比較,S組大鼠體重、血清TG低于F組(P0.05)；S+E、S+L、S+E+L組大鼠體重、血清TG低于F組,同時低于S組(P0.05)；S+L、S+E+L組血清TC、肝臟TG水平低于F組(P0.05)；S+E+L組內臟脂肪系數(shù)低于F組,血清HDL水平高于F組(P0.05)。 3.S組大鼠肝臟PPARα、PGC-1α、AMPKα2、CPT1、MCAD的基因及蛋白水平與F組無顯著差異(P0.05); S+E、S+L、S+E+L組的PPARα、PGC-1α、AMPKα2、 CPT1、MCAD的基因及/蛋白水平較F組有顯著差異(P0.05); S+E、S+L、S+E+L組的CPTlmRNA顯著高于S組(P0.05)；S+E+L組大鼠的PPARα、PGC-1α、AMPK α2、MCADmRNA顯著高于S+E和/或S+L組(P0.05)。 結論： 1.肥胖大鼠AMPKα2表達下降,PGC-1α、PPARα的表達減弱,同時PPAR α介導的下游靶基因CPT1轉錄和翻譯活性下降； 2.運動可以減肥,EGCG、肉堿和兩者聯(lián)用可增強運動減肥的作用,PPARα、PGC-1α、AMPKα2、CPT1、MCAD因子改變可能是其機制之一。
[Abstract]:Aim: to study the effects of exercise, EGCG and carnitine on weight loss, lipid metabolism and gene expression in obese rats, and to explore the molecular mechanism of simple obesity. Methods: the obese rat model was established. The effects of high-fat diet on body weight, visceral fat coefficient, TGG TC HDL concentration, tissue TGG, liver PPAR 偽 PGC-1 偽 AMPK 偽 2AMPK 偽 2 and CPT1MCAD expression were studied. It was divided into obesity control group, exercise EGCG group, exercise carnitine group, exercise EGCG intervention group, and exercise EGCG carnitine intervention group. Except for F group, the other four groups were given low intensity aerobic treadmill training. Body weight, visceral fat coefficient, serum TGG TU HDL concentration, tissue TG level, liver PPAR 偽 PGC-1 偽 AMPK 偽 2 and CPT1MCAD gene and protein levels were measured after the experiment. Results: 1. Serum TGN TC in group F was higher than that in control group (P 0.05), TG in liver was higher than that in group C (P 0.05), PPAR 偽 mRNA and protein PGC-1 偽 mRNAAMPK a2 protein were significantly lower than those in group C (P 0.05); 2. Compared with group F, the body weight, serum TG and liver TG of S group were lower than those of F group and F group, respectively. The serum TG was lower than that of F group, and that of S group was lower than that of S group, and the level of liver TG was lower than that of F group. The visceral fat coefficient in S E L group was lower than that in F group. The level of serum HDL was higher than that of group F (P0.05). 3.The gene and protein levels of PPAR 偽 PGC-1 偽 AMPK 偽 2 and CPT1MCAD in liver of group S were not significantly different from those of group F (P 0.05), and the levels of gene and / protein of PPAR 偽 PGC-1 偽 AMPK 偽 and CPT1 MCAD in group S were significantly higher than those in group F (P 0.05), and the gene and / protein levels of PPAR 偽 PGC-1 偽 AMPK 偽 and CPT1MCAD in group S were significantly higher than those in group F (P < 0.05), and the gene and protein levels of PPAR 偽 PGC-1 偽 AMPK 偽 and CPT 1 in group C were significantly higher than those in group F. CPTL mRNA in group S was significantly higher than that in group S (P 0.05). Compared with S E and / or S L group, the mRNA of PPAR 偽 PGC-1 偽 AMPK 偽 2 mCAD was significantly higher in S El group than that in S E and / or S L group (P 0.05). Conclusion: 1. In obese rats, the expression of AMPK 偽 2 decreased and the expression of PGC-1 偽 PPAR 偽 decreased, while the down-stream target gene CPT1 transcriptional and translation activity of PPAR 偽 decreased; 2. Exercise can reduce weight by EGCG, carnitine and the combination of them can enhance exercise weight loss. The change of PPAR 偽 -PGC-1 偽 AMPK 偽 2- CPT1MCAD may be one of its mechanisms.
【學位授予單位】：北京體育大學
【學位級別】：博士
【學位授予年份】：2012
【分類號】：G804.2

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本文編號：2035561