运动和EGCG、肉碱对肥胖大鼠减肥和脂代谢及基因表达的影响
发布时间:2018-06-18 12:57
本文选题:肥胖 + 运动 ; 参考:《北京体育大学》2012年博士论文
【摘要】:目的: 研究运动和EGCG、肉碱对单纯性肥胖大鼠减肥和脂代谢及基因表达的作用,并探讨单纯性肥胖发生的分子学机制。 方法: 建立肥胖大鼠模型。研究8周高脂饮食对其体重、内脏脂肪系数、血清TG、TC HDL浓度、组织TG、肝脏PPARα、PGC-1α、AMPKα2、CPT1、MCAD表达水平的影响,然后随机选取肥胖造模成功大鼠30只进行减肥干预实验,将其分为肥胖对照组(F),运动组(S),运动+EGCG组(S+E),运动+肉碱组(S+L),运动+EGCG+肉碱干预组(S+E+L),除F组外,其他四组大鼠进行低强度有氧跑台训练。实验结束后测试各组大鼠的体重、内脏脂肪系数、血清TG、T、HDL浓度、组织TG水平、肝脏PPARα、PGC-1α、AMPKα2、CPT1、MCAD的基因及蛋白水平。 结果: 1.F组血清TG、TC高于正常对照组(C),HDL低于C组(P0.05);肝脏TG较C组高(P0.05); PPARαmRNA及蛋白、PGC-1αmRNA、AMPK a2蛋白显著低于C组.(P0.05); 2.与F组比较,S组大鼠体重、血清TG低于F组(P0.05);S+E、S+L、S+E+L组大鼠体重、血清TG低于F组,同时低于S组(P0.05);S+L、S+E+L组血清TC、肝脏TG水平低于F组(P0.05);S+E+L组内脏脂肪系数低于F组,血清HDL水平高于F组(P0.05)。 3.S组大鼠肝脏PPARα、PGC-1α、AMPKα2、CPT1、MCAD的基因及蛋白水平与F组无显著差异(P0.05); S+E、S+L、S+E+L组的PPARα、PGC-1α、AMPKα2、 CPT1、MCAD的基因及/蛋白水平较F组有显著差异(P0.05); S+E、S+L、S+E+L组的CPTlmRNA显著高于S组(P0.05);S+E+L组大鼠的PPARα、PGC-1α、AMPK α2、MCADmRNA显著高于S+E和/或S+L组(P0.05)。 结论: 1.肥胖大鼠AMPKα2表达下降,PGC-1α、PPARα的表达减弱,同时PPAR α介导的下游靶基因CPT1转录和翻译活性下降; 2.运动可以减肥,EGCG、肉碱和两者联用可增强运动减肥的作用,PPARα、PGC-1α、AMPKα2、CPT1、MCAD因子改变可能是其机制之一。
[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 伪 PGC-1 伪 AMPK 伪 2AMPK 伪 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 伪 PGC-1 伪 AMPK 伪 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 伪 mRNA and protein PGC-1 伪 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 伪 PGC-1 伪 AMPK 伪 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 伪 PGC-1 伪 AMPK 伪 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 伪 PGC-1 伪 AMPK 伪 and CPT1MCAD in group S were significantly higher than those in group F (P < 0.05), and the gene and protein levels of PPAR 伪 PGC-1 伪 AMPK 伪 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 伪 PGC-1 伪 AMPK 伪 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 伪 2 decreased and the expression of PGC-1 伪 PPAR 伪 decreased, while the down-stream target gene CPT1 transcriptional and translation activity of PPAR 伪 decreased; 2. Exercise can reduce weight by EGCG, carnitine and the combination of them can enhance exercise weight loss. The change of PPAR 伪 -PGC-1 伪 AMPK 伪 2- CPT1MCAD may be one of its mechanisms.
【学位授予单位】:北京体育大学
【学位级别】:博士
【学位授予年份】:2012
【分类号】:G804.2
【参考文献】
相关期刊论文 前4条
1 周书凤,何志谦,刘建平,佘辉;左旋肉碱对肥胖青少年体重综合性控制的影响[J];营养学报;1997年02期
2 殷峻,陈名道,杨颖,唐金凤,李凤英;小檗碱对大鼠脂代谢的影响[J];上海第二医科大学学报;2003年S1期
3 宋小鸽,唐照亮,侯正明,袁静,章复清,陈全珠,刘先华;茶多酚对大鼠高脂血症的预防作用[J];中医研究;1998年01期
4 周e吋,
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