Suchergebnisse

AbstractIn this ongoing longitudinal study of adolescent twins/sibling pairs and their parents in Taipei, we aimed to investigate the genetic and environmental influences on adolescent behavioral development, metabolic risk factors, and the associations between the two. Special focus is on anxious depression, metabolic profile, and hormonal factors such as cortisol and leptin. The first wave of assessment was completed during the period of 2002 to 2005 and included 192 twin pairs, 6 triplets, 56 sibling pairs and their first-degree relatives (484 parents and 142 siblings). We are currently in the process of a second wave assessment as follow-up. Dimensional psychological assessments using self-report questionnaires, as well as categorical assessments based on semistructured clinical interviews, were performed. All subjects received a 2-hour oral glucose tolerance test at the examination site. The metabolic phenotypes including body mass index, blood pressure, levels of glucose, insulin, and lipid profile as well as related hormonal levels were measured. Zygosity was determined using DNA, except for a few twins whose DNA was not available. Such a combination of detailed psychological assessments and metabolic function tests is expected to help shed light on the interrelation of psychological well-being and metabolic functioning.

AbstractCirculating 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.