运动对生长期大鼠脂肪组织FTO及相关基因表达的影响

发布时间：2018-03-01 13:19

本文关键词： 生长期 FTO 脂代谢有氧运动　出处：《北京体育大学》2017年硕士论文　论文类型：学位论文

【摘要】：研究目的:通过观察生长发育突增期的运动干预(4周)和长期有氧运动干预(12周)对大鼠脂肪组织FTO及相关基因表达的影响,初步探讨运动调控脂肪代谢的分子分子生物学机制。研究方法:3周龄SD雄性大鼠40只,随机分为对照组(C4、C12)和4、12周运动组(E4、E12),每组各10只。E4组、E12组分别进行4周、12周跑台运动,强度为60%VO2max,跑台速度根据每两周最大摄氧量的测定结果调整。每周训练5天,每天1小时。每周记录大鼠体重和摄食量。测定训练后安静禁食状态下大鼠的血脂,肾周和附睾脂肪组织重量。RT-PCR法测定脂肪组织FTO、C/EBPβ、PPARγ、FAS、Perilipin、HSL mRNA的表达量。western blot法测定大鼠脂肪组织中FTO、C/EBPβ、PPARγ的蛋白含量。结果:1、随着周龄的增加,4组大鼠体重均在不断增长。在各对应时间点上,从运动第二周开始,E4组大鼠的体重均显著低于C4组,直到4周运动结束;E12组大鼠体重显著低于C12组,直到第12周运动结束;2、E4、E12组大鼠内脏脂肪绝对重量和相对重量均分别显著低于C4、C12组;3、E4组大鼠血清LDL-C浓度显著低于C4组大鼠,血清HDL-C浓度显著高于C4组大鼠;E12组大鼠血清TG、LDL-C浓度显著低于C12组,血清HDL-C浓度显著高于C12组;4、E4组大鼠脂肪组织FTO、PPARγ的蛋白含量显著低于C4组,C/EBPβ、PPARγ、FAS、Perlipin mRNA表达量显著低于C4组,HSL mRNA表达量显著高于C4组;E12组大鼠脂肪组织FTO、C/EBPβ、PPARγ、FAS、Perilipin mRNA表达量均显著低于C12组。结论:1.生长发育突增期(4周)的有氧运动干预通过下调脂肪组织FTO、PPARγ、FAS基因表达抑制脂肪细胞分化和脂肪合成,促进脂肪分解基因Perilipin和HSL发挥作用,降低大鼠体重和脂体比。2.长期有氧运动干预(12周)通过下调FTO、C/EBPβ、PPARγ、FAS mRNA水平,抑制脂肪合成,降低大鼠体重和体脂比。
[Abstract]:Objective: to observe the effects of exercise intervention (4 weeks) and long-term aerobic exercise intervention (12 weeks) on the expression of FTO and related genes in adipose tissue of rats. Methods Forty male Sprague-Dawley rats at the age of 3 weeks were randomly divided into two groups: the control group (C4C12) and the 44-week exercise group (E4C12). Each group (10 rats in each group) and E12 group (E12 group) underwent treadmill exercise for 4 weeks and 12 weeks respectively. The running speed was adjusted according to the results of the maximal oxygen intake every two weeks. The rats were trained for 5 days a week for 1 hour a day. The body weight and food intake of the rats were recorded weekly. The blood lipids of the rats in the state of quiet fasting after training were measured. The expression of FTOC / EBP 尾 -PPAR- 尾 PPAR- PPAR- 尾 -PPAR- perilipinia mRNA in adipose tissue was measured by RT-PCR. Western blot method was used to determine the protein content of FTOC- EBP 尾 -PPAR- 纬 in adipose tissue of rats. Results the weight of rats in groups 1 and 4 increased with the increase of week age. At each corresponding time point, the protein content of FTOC / EBP 尾 -PPAR- 纬 in rat adipose tissue was determined by Western blot. From the second week of exercise, the weight of group E _ 4 was significantly lower than that of group C _ 4, and the body weight of group E12 was significantly lower than that of group C _ 12 at the end of 4-week exercise. At the end of the 12th week of exercise, the absolute and relative weight of visceral fat in group E12 was significantly lower than that in group C _ (4) C _ (12) and in group C _ (3) C _ (4) E _ (4) E _ (4), and the serum LDL-C concentration in group C _ 4 was significantly lower than that in group C _ 4. The serum HDL-C level was significantly higher than that of C 4 group and C 12 group, and it was significantly lower than that of C 12 group, and that of C 12 group was significantly lower than that of C 12 group. The level of serum HDL-C was significantly higher than that of C12 group and C12 group. The protein content of HDL-C 纬 in adipose tissue was significantly lower than that in C4 group. It was significantly lower than that in C4 group. It was significantly lower than that in C 4 group and C 4 group. It was significantly higher than that in C 4 group E12 group and C 4 group E12 group. All of them were significantly lower than those in C 4 group and C 4 group. Conclusion the aerobic exercise intervention can inhibit adipocyte differentiation and adipose synthesis by down-regulating the expression of FTO- PPAR 纬 -FAS gene in adipose tissue. The effects of Perilipin and HSL on the lipid synthesis and the ratio of body weight and fat to body weight of rats were decreased, and the ratio of body weight to body fat was decreased by long-term aerobic exercise for 12 weeks.) through the down-regulation of FTOV C / EBP 尾 -PPAR- 纬 mRNA level, fat synthesis was inhibited and the ratio of body weight to body fat was decreased.
【学位授予单位】：北京体育大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：G804.2

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