Genetic and Environmental Influences on Adiponectin, Leptin, and BMI Among Adolescents in Taiwan: A Multivariate Twin/Sibling Analysis
Genetic and Environmental Influences on Adiponectin, Leptin, and BMI Among Adolescents in Taiwan: A Multivariate Twin/Sibling Analysis
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DOI：
10.1375/twin.11.5.495
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发表时间：
2008-10-01
影响因子：
0.9
通讯作者：
Chuang, Lee-Ming
中科院分区：
文献类型：
--
作者：
Liu, Pi-Hua;Jiang, Yi-Der;Chuang, Lee-Ming
瘦素和脂联素的循环水平与肥胖密切相关。然而，是否存在共同的共享基因或环境对瘦素、脂联素和BMI水平产生影响尚不清楚。我们的目的是评估基因和环境的相对贡献脂联素，瘦素，BMI单独以及同时对三个措施。研究对象为228对12 ~ 18岁的双胞胎/兄弟姐妹，其中同卵双胞胎130对，异卵双胞胎68对，兄弟姐妹30对。采用结构方程模型对双胞胎/同胞数据进行多变量分析。结果表明，脂联素、瘦素和BMI的组内相关性在MZ双胞胎中高于DZ/SP组。基因对脂联素的相对贡献（39%）与共享环境的基因贡献（40%）相当。相比之下，瘦素和BMI主要受基因影响（分别为74%和89%）。多变量遗传分析表明，潜在的因素的三个措施被确定，与体重指数相当于这个潜在的因素。BMI依赖的遗传因素只能分别解释脂联素和瘦素变异的15%和34%。这些数据表明遗传因素对脂联素、瘦素和BMI的变化有不同的贡献。更重要的是，只有一小部分对脂联素和瘦素的遗传影响归因于BMI。我们的研究结果为脂联素和瘦素在肥胖中的复杂调节提供了更多的见解。
Circulating levels of leptin and adiponectin are closely associated with obesity. However, it is not known whether there are common shared genes or environment exerting influences on the levels of leptin, adiponectin, and BMI. We aimed to assess the relative contribution of genes and environment to adiponectin, leptin, and BMI individually as well as simultaneously to the three measures. Our subjects included a total of 228 twin/sibling pairs aged 12 to 18 (130 monozygotic twins, 68 dizygotic twins and 30 sibling pairs) were recruited from the middle schools. Multivariate analyses were applied to twin/sibling data using structural equation modeling. The results showed that intraclass correlations for adiponectin, leptin and BMI were higher in the MZ twins than those in the DZ/SP group. The relative contribution of genes to adiponectin (39%) was comparable to those of shared environment (40%). In contrast, leptin and BMI were influenced mostly by genes (74% and 89%, respectively). The multivariate genetic analyses showed that a latent factor underlying the three measures was identified, with BMI being equivalent to this latent factor. The BMI-dependent genetic factor explains only 15% and 34% of variation of adiponectin and leptin, respectively. These data indicate a differential contribution of genetic factors for the variation of adiponectin, leptin and BMI. More importantly, only a small portion of the genetic influences on adiponectin and leptin was attributed to BMI. Our findings provided more insight into the complex regulation of adiponectin and leptin in obesity.