摘要
目的:探讨肥胖儿童少年内脂素RS4730153位点基因多态性及其与运动干预引起糖代谢和脂代谢变化的关系。方法:对88名年龄为144.11±3.63岁,BMI为29.26±4.44的汉族肥胖儿童少年(男40名,女48名)进行封闭式的4周中等强度有氧运动减肥,LDR-PCR测序分型技术确定受试者内脂素RS4730153位点基因型,并在运动干预前后进行糖代谢和脂代谢指标的测定。结果:受试者A/G基因型出现频率为15.9%,有氧运动前后各指标呈显著性变化,不同基因型受试者运动前TG水平呈显著性差异(分别为GG:1.40±0.74mmol/L;AG:1.86±1.11mmol/L;P=0.050),运动引起的不同基因型受试者HOMA-β变化差异显著(P=0.050)。结论:所测中国汉族肥胖儿童少年中存在内脂素单核苷酸多态性位点RS4730153变异,RS4730153纯合子GG型可能可以通过降低TG水平、提高胰岛素对运动干预的敏感性等方面参与肥胖儿童少年的糖代谢和脂代谢调节。
Objective:To investigate the single nucleotide polymorphisms (SNPs) of RS4730153 in visfatin gene in obese children and adolescents of Han nationality,and analyze its relation to the exercise-induced glucose and lipid metabolism changes.Methods:88 obese children and adolescents (male=40,female=48;age=14.11±3.63;BMI=29.26±4.44) of Han nationality completed a 4-week aerobic exercise program to lose weight,and their distribution of genotype was got by using ligase detection-polymerase chain reaction (LDR-PCR).Meanwhile,the indexes of glucose and lipid metabolism before and after exercise intervention were determined.Results:The frequency of the visfatin A/G genotype was 15.9%.The indexes of glucose and lipid metabolism before and after aerobic exercise showed significant changes.TG levels before exercise was significantly different between the different genotypes subjects (GG:1.40±0.74mmol / L,AG:1.86±1.11mmol / L,respectively,P=0.050).HOMA-β after exercise was significantly different between the different genotypes subjects (GG:220.50±178.81,AG:332.23±207.90,respectively,P=0.050).Conclusion:The SNPs of visfatin RS4730153 variation was found in obesity children and adolescents from Chinese Han nationality.Homozygous GG was possibly involved in glucose and lipid metabolism by reducing TG levels and improving exercise-induced insulin sensitivity.
出处
《体育科学》
CSSCI
北大核心
2010年第8期57-61,共5页
China Sport Science
基金
国家科技支撑计划项目(2006BAK33B04-2)
上海市第三期运动人体科学重点学科开放基金课题(S30902)
关键词
内脂素
基因多态
肥胖儿童少年
糖代谢
脂代谢
visfatin
single nucleotide polymorphisms (SNPs)
obese children and adolescents
glucose and lipid metabolism