β_3-肾上腺素能受体基因突变与肥胖儿童膳食干预效果

为分析 β3 肾上腺素能受体 (β3 adr)基因突变与单纯性肥胖儿童对膳食干预应答差异的关系 ,将 47名单纯性肥胖儿童随机分为膳食干预组 (36名 )和对照组 (11名 ) ,膳食干预期 3个月 ,干预前后分别进行膳食调查和体格测量。所有研究对象均采用PCR RFLP方法检测 β3 肾上腺素能受体 (β3 adr)基因中编码多肽链第 6 4位的色氨酸密码子被精氨酸密码子 (Trp6 4Arg)取代的突变。结果显示 ,这 47名肥胖儿童膳食结构中脂肪供能过高 ,占 40 7% ;膳食干预后 ,在膳食干预组中无 β3 adr基因Trp6 4Arg突变者的体重、体质指数(BMI)增长幅度低于非膳食干预组 (P <0 0 5 ) ,而有突变者的体重、BMI增长幅度与非膳食干预组相比 ,则不存在统计学差异。结论认为 β3 adr基因Trp6 4Arg突变可能是单纯性肥胖儿童膳食干预效果较差的原因之一。

Mutation of beta 3-adrenergic-receptor gene and the response to dietary intervention in obese children]

In order to study the relationship between mutation of beta 3-adrenergic-receptor gene and the response to dietary intervention in obese children, 47 obese children were randomly separated into two groups. One was dietary intervention group(36 subjects); the other was control group(11 subjects). The subjects were investigated by dietary survey and anthropometry before and after dietary intervention carried out for 3 months. The mutation of beta 3-adrenergic receptor gene resulting from the replacement of tryptophan by arginine at position 64(Trp64Arg) in encoding amino acid residues was detected by using a polymerase chain reaction-restriction fragment length polymorphisms. The results showed that dietary fat was higher (40.7% of energy from fat) in the obese children. After dietary intervention, the increase of weight(kg) and BMI(kg/m2) were significantly lower in the obese children without mutation than in control group(P < 0.05), but the changes of weight and BMI in the obese children with mutations were similar to those of control group. It was concluded that the Trp64Arg mutation of beta 3-adrenergic receptor gene might be one of the reasons why the effect of dietary intervention was poor in some obese children.