不同强度耐力运动影响高脂诱导肥胖模型小鼠血清Irisin含量、骨骼肌PGC-1α、FNDC5、PPARδ蛋白的表达
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摘要
背景:研究表明小鼠体内过氧化物酶体增殖活化受体γ辅助活化因子1α(peroxisome proliferators-activated receptor-γcoactivator-1α,PGC-1α)蛋白、Ⅲ型纤维连接蛋白域蛋白5(fibronectin typeⅢdomain-containing protein 5,FNDC5)蛋白和Irisin组成一条正向调节脂肪分解代谢的通路,并且PGC-1α能调控骨骼肌中调节脂肪代谢相关蛋白PPARδ的表达。耐力运动训练可以有效减轻小鼠体质量,但不同强度耐力运动训练对高脂诱导的肥胖小鼠血清Irisin含量及骨骼肌中PGC-1α、FNDC5、PPARδ蛋白表达的影响尚不清楚。目的:分析不同强度耐力运动训练对高脂诱导肥胖小鼠血液中Irisin含量及骨骼肌中脂肪代谢相关蛋白的影响。方法:4周龄雄性C57BL/6J小鼠经过1周常规饲料适应性喂养后,通过8周高脂饲料喂养建立营养性肥胖小鼠模型,对照小鼠一直使用常规饲料喂养。构建成功的肥胖小鼠经过1周适应性跑台运动后,分为高强度耐力运动组和低强度耐力运动组进行跑台运动,对照小鼠不运动。8周后量小鼠体长、称量体质量并计算Lee’s指数,同时取各组小鼠血清和股四头肌,使用ELISA方法检测小鼠血清中Irisin水平并对比各组变化,使用Western Blot方法检测小鼠股四头肌中PGC-1α、FNDC5和PPARδ蛋白的表达情况并对比各组变化。结果与结论:①高脂诱导能够明显增大小鼠的体长、体质量和Lee’s指数,表明高脂诱导的营养性肥胖小鼠模型是成功的,并且高脂诱导能明显降低小鼠血清Irisin水平,降低小鼠股四头肌脂质代谢相关蛋白PGC-1α、FNDC5和PPARδ的表达;②耐力运动训练尤其是高强度耐力运动训练能有效减小肥胖小鼠体长、体质量和Lee’s指数;③耐力运动训练尤其是高强度耐力运动训练能有效提高肥胖小鼠血清中Irisin水平,明显提高小鼠股四头肌PGC-1α、FNDC5和PPARδ蛋白的表达;④ PGC-1α和FNDC5蛋白与Irisin的变化一致,提示耐力运动训练尤其是高强度耐力运动训练可以诱导骨骼肌高表达PGC-1α蛋白,从而促进FNDC5蛋白高表达,随着FNDC5蛋白在体内被剪切转变成高浓度的Irisin释放到血液中,加速小鼠脂肪代谢水平,达到减肥的目的。
BACKGROUND: Peroxisome proliferators-activated receptor-γ coactivator-1 alpha(PGC-1α), fibronectin type III domain-containing protein 5(FNDC5) and Irisin in mice have been shown to make a positive pathway of lipolysis, and PGC-1α can regulate the expression of peroxisome proliferator-activated receptor delta(PPARδ), which regulates lipolysis in skeletal muscle. Endurance training can effectively reduce the body mass of mice, but the effect of different intensities of endurance training on serum Irisin level, and PGC-1α, FNDC5, PPARδ expression in mice with obesity induced by a high fat diet is still unclear. OBJECTIVE: To study the effect of high-and low-intensity endurance training on serum Irisin level, and lipolysis-related proteins in mice with obesity induced by a high fat diet. METHODS: Four-week-old male C57 BL/6 J mice were fed normal diet for 1 week and then fed 8 weeks of high-fat diet to establish a mouse model of nutritional obesity. The control mice were fed a normal diet. After 1 week of adaptive treadmill training, the obese mice were divided into high-and low-intensity endurance training groups for treadmill training and the control group had no training. After 8 weeks, the body length, body mass and Lee's index were measured and recorded. The level of Irisin in mouse serum was detected by ELISA. The expression levels of PGC-1α, FNDC5 and PPARδ in quadriceps femoris were detected by western blot assay. RESULTS AND CONCLUSION: High-fat diet could significantly increase body length, body mass and Lee's index of mice, suggesting that high-fat-induced nutritional obesity mouse model was established. High-fat diet could significantly reduce the level of Irisin in serum and the expression of lipolysis-related proteins PGC-1α, FNDC5 and PPARδ in quadriceps femoris. Endurance training, especially high-intensity endurance training could effectively reduce the body length, body mass and Lee's index of mice. Endurance training, especially high-intensity endurance training could effectively increase the level of Irisin in serum and the expression of PGC-1α, FNDC5 and PPARδ in quadriceps femoris. PGC-1α, FNDC5 and Irisin have consistent expression, suggesting that endurance training, especially high-intensity endurance training can up-regulate the expression of skeletal muscle PGC-1α, thereby increasing the expression of FNDC5 protein. FNDC5 is transformed into Irisin and released into the blood, thus increasing the level of lipolysis in mice, and achieving weight loss.
BACKGROUND: Peroxisome proliferators-activated receptor-γ coactivator-1 alpha(PGC-1α), fibronectin type III domain-containing protein 5(FNDC5) and Irisin in mice have been shown to make a positive pathway of lipolysis, and PGC-1α can regulate the expression of peroxisome proliferator-activated receptor delta(PPARδ), which regulates lipolysis in skeletal muscle. Endurance training can effectively reduce the body mass of mice, but the effect of different intensities of endurance training on serum Irisin level, and PGC-1α, FNDC5, PPARδ expression in mice with obesity induced by a high fat diet is still unclear. OBJECTIVE: To study the effect of high-and low-intensity endurance training on serum Irisin level, and lipolysis-related proteins in mice with obesity induced by a high fat diet. METHODS: Four-week-old male C57 BL/6 J mice were fed normal diet for 1 week and then fed 8 weeks of high-fat diet to establish a mouse model of nutritional obesity. The control mice were fed a normal diet. After 1 week of adaptive treadmill training, the obese mice were divided into high-and low-intensity endurance training groups for treadmill training and the control group had no training. After 8 weeks, the body length, body mass and Lee's index were measured and recorded. The level of Irisin in mouse serum was detected by ELISA. The expression levels of PGC-1α, FNDC5 and PPARδ in quadriceps femoris were detected by western blot assay. RESULTS AND CONCLUSION: High-fat diet could significantly increase body length, body mass and Lee's index of mice, suggesting that high-fat-induced nutritional obesity mouse model was established. High-fat diet could significantly reduce the level of Irisin in serum and the expression of lipolysis-related proteins PGC-1α, FNDC5 and PPARδ in quadriceps femoris. Endurance training, especially high-intensity endurance training could effectively reduce the body length, body mass and Lee's index of mice. Endurance training, especially high-intensity endurance training could effectively increase the level of Irisin in serum and the expression of PGC-1α, FNDC5 and PPARδ in quadriceps femoris. PGC-1α, FNDC5 and Irisin have consistent expression, suggesting that endurance training, especially high-intensity endurance training can up-regulate the expression of skeletal muscle PGC-1α, thereby increasing the expression of FNDC5 protein. FNDC5 is transformed into Irisin and released into the blood, thus increasing the level of lipolysis in mice, and achieving weight loss.
引文
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[2]倪国华,张璟,郑风田.中国肥胖流行的现状与趋势[J].中国食物与营养,2013,19(10):70-74.
[3]Strasser B.Physical activity in obesity and metabolic syndrome.Ann N Y Acad Sci.2013;1281:141-159.
[4]Matsunaga Y,Tamura Y,Sakata Y,et al.Comparison between pre-exercise casein peptide and intact casein supplementation on glucose tolerance in high-fat diet-fed mice.Appl Physiol Nutr Metab.2017;1.
[5]Wang N,Liu Y,Ma Y,et al.High-intensity interval versus moderate-intensity continuous training:Superior metabolic benefits in diet-induced obesity mice.Life Sci.2017;15(191):122-131.
[6]Bae JY,Woo J,Roh HT,et al.The effects of detraining and training on adipose tissue lipid droplet in obese mice after chronic high-fat diet.Lipids Health Dis.2017;16(1):13.
[7]Marques CM,Motta VF,Torres TS,et al.Beneficial effects of exercise training(treadmill)on insulin resistance and nonalcoholic fatty liver disease in high-fat fed C57BL/6 mice.Braz J Med Biol Res.2010;43(5):467-475.
[8]Chiu CH,Ko MC,Wu LS,et al.Benefits of different intensity of aerobic exercise in modulating body composition among obese young adults:a pilot randomized controlled trial.Health Qual Life Outcomes.2017;15(1):168.
[9]Puigserver P,Wu Z,Park CW,et al.A cold-inducible coactivator of nuclear receptors linked to adaptive thermogenesis.Cell.998;92:829-839.
[10]Bostrom P,Wu J,Jedrychowski MP,et al.A PGC1-α-dependent myokine that drives brown-fat-like development of white fat and thermogenesis.Nature.2012;481(7382):463-468.
[11]Lira VA,Benton CR,Yan Z,et al.PGC-1αregulation by exercise training and its influences on muscle function and insulin sensitivity.Am J Physiol Endocrinol Metab.2010;299:145-161.
[12]Yan Z,Li P,Akimoto T.Transcriptional control of the Pgc-1αgene in skeletal muscle in vivo.Exerc Sport Sci Rev.2007;35(3):97-101.
[13]Lopaschuk GD,Belke DD,Gamble J,et al.Regulation of fatty acid oxidation in the mammalian heart in health and disease.Biochim Biophys Acta.1994;1213(4):263-276.
[14]Hondares E,Torra IP,Iglesias R,et al.PPARδ,but not PPARα,activates PGC-1αgene transcription in muscle.Biochemical and Biophysical Research Communications.2007;354:1021-1027.
[15]Luquet S,Lopez-Soriano J,Holst D,et al.Peroxisome proliferator-activated receptorδcontrols muscle development and oxydative capability.FASEB J.2003;17(15):2299-2301.
[16]Wang Y,Lee CH,Tiep S,et al.Peroxisome-proliferator-activated receptorδactivates fat metabolism to prevent obesity.Cell.2003;113(2):159-170.
[17]Dressel U,Allen TL,Pippal JB,et al.The Peroxisome Proliferator-Activated Receptorβ/δAgonist,GW501516,Regulates the Expression of Genes Involved in Lipid Catabolism and Energy Uncoupling in Skeletal Muscle Cells.Mol Endocrinol.2003;17(12):2477-2493.
[18]Roberts MD,Bayless DS,Company JM,et al.Elevated skeletal muscle irisin precursor FNDC5 mRNA in obese OLETF rats.Metabolism.2013;62(8):1052-1056.
[19]Swick AG,Orena S,O'Connor A.Irisin levels correlate with energy expenditure in a subgroup of humans with energy expenditure greater than predicted by fat free mass.Metabolism.2013;62(8):1070-1073.
[20]Handschin C,Chin S,Li P,et al.Skeletal muscle fiber-type switching,exercise intolerance,and myopathy in PGC-1αmuscle-specific knock-out animals.J Biol Chem.2007;282:30014-30021.
[21]Camargo GL,de Souza RA,da Silva DB,et al.Raman spectral characteristics of neck and head of femur in low-density lipoprotein receptor gene knockout mice submitted to treadmill aerobic training.J Photochem Photobiol B.2017;173:92-98.
[22]朱小烽,王茹,杨钦,等.不同强度急性有氧运动对肥胖小鼠PGC-1α及其下游因子的调控影响[J].体育科学,2017,37(3):44-50.
[23]Kus V,Prazak T,Brauner P,et al.Induction of muscle thermogenesis by high-fat diet in mice:association with obesity-resistance.Am J Physiol Endocrinol Metab.2008;295(2):E356-E367.
[24]Wang B,Sun J,Ma Y,et al.Increased oxidative stress and the apoptosis of regulatory T cells in obese mice but not resistant mice in response to a high-fat diet.Cell Immunol.2014;288(1-2):39-46.
[25]王欢,李宛真,汪弋力,等.高脂饮食诱导的肥胖及肥胖抵抗小鼠肠道菌群元基因组的比较研究[J].西安交通大学学报(医学版),2014,35(2):240-244.
[26]Timmons JA,Baar K,Davidsen PK,et a1.Is irisin a human exercise gene?Nature.2012;488(7413):E9-E10.
[27]Chen J,Huang Y,Gusdon AM,et al.Irisin:a new molecular marker and target in metabolic disorder.Lipids Health Dis.2015;14:2.
[28]Huh JY,Panagiotou G,Mougios V,et al.FNDC5 and irisin in humans:I.Predictors of circulating concentrations in serum and plasma and II.mRNA expression and circulating concentrations in response to weight loss and exercise.Metabolism.2012;61(12):1725-1738.
[29]Stengel A,Hofmann T,Goebel-Stengel M,et al.Circulating levels of irisin in patients with anorexia nervosa and different stages of obesity-correlation with body mass index.Peptides.2013;39:125-130.
[30]Crujeiras AB,Pardo M,Arturo RR,et al.Longitudinal variation of circulating irisin after an energy restriction-induced weight loss and following weight regain in obese men and women.Am J Hum Biol.2014;26(2):198-207.
[31]Choi YK,Kim MK,Bae KH,et al.Serum irisin levels in new-onset type 2 diabetes.Diabetes Res Clin Pract.2013;100(1):96-101.
[32]Moreno-Navarrete JM,Ortega F,Serrano M,et al.Irisin is expressed and produced by human muscle and adipose tissue in association with obesity and insulin resistance.J Clin Endocrinol Metab.2013;98(4):E769-778.
[33]Lecker SH,Zavin A,Cao P,et al.Expression of the irisin precursor FNDC5 in skeletal muscle correlates with aerobic exercise performance in patients with heart failure.Circ Heart Fail.2012;5(6):812-818.
[34]Mahmoodnia L,Sadoughi M,Ahmadi A,et al.Relationship between serum irisin,glycemic indices,and renal function in type 2 diabetic patients.J Renal Inj Prev.2017;6(2):88-92.
[35]Rohas LM,St-Pierre J,Uldry M,et al.A Fundamental System of Cellular Energy Homeostasis Regulated by PGC-1α.Proc Natl Acad Sci.U.S.A.2007;104(19):7933-7938.
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