|Cai, Guowen - SWFBR, SAN ANTONIO|
|Tejero, Maria - SWFBR, SAN ANTONIO|
|Cole, Shelley - SWFBR, SAN ANTONIO|
|Mehta, Nitesh - BAYLOR COLLEGE MED|
|Comuzzie, Anthony - SWFBR, SAN ANTONIO|
Submitted to: Obesity Research
Publication Type: Abstract Only
Publication Acceptance Date: August 18, 2004
Publication Date: October 1, 2004
Citation: Cai, G., Tejero, M., Cole, S., Mehta, N.R., Butte, N.F., Comuzzie, A. 2004. Evidence of pleiotropy between obesity and other phenotypes related to the metabolic syndrome in children. Obesity Research. S12(10):A194. Interpretive Summary: Not required for an abstract.
Technical Abstract: As observed in adults, the increase in the prevalence of childhood obesity seems to be associated with the escalation of abnormalities that characterize the metabolic syndrome. The aim of this study was to identify the genetic effects on obesity and the metabolic syndrome related phenotypes in children. The sample consisted of Hispanic families with at least one overweight child and their siblings. Blood was collected under fasting conditions for analyses of levels of glucose, triglycerides, non-esterified fatty acids (NEFA), adiponectin, insulin and C-peptide using reference methods. Weight, height, waist and hip circumferences were measured. Univariate and bivariate quantitative genetic analyses were conducted using the variance decomposition approach implemented in SOLAR. Circulating levels of glucose, triglycerides, insulin, HOMA index, C-peptide, NEFA and adiponectin had significant heritabilities with values ranging from h2=0.17 to 0.82. Significant genetic correlations were calculated between the weight Z-score and insulin (RHO G=0.51, p=0.05), C-peptide (RHO G=0.38, p=0.05), HOMA index (RHO G=0.52, p=0.036), adiponectin (RHO G = -0.33, p=0.05) and leptin (RHO G=0.68, p=0.002), levels of adiponectin and HOMA-IR (RHO G = -0.44, p=0.00003), adiponectin and insulin (RHO G = -0.49, p=0.02), and leptin and C-peptide (RHO G=0.49, p=0.012). Environmental correlations were observed between adiponectin levels and HOMA index (RHO E = -0.37, p=0.0001), C-peptide (RHO E = -0.43, p=0.000) and insulin (RHO E = -0.49, p=0.02). A significant contribution of genes to the analyzed traits was observed in these children as in adults. These data suggest that a common set of genes influence the weight Z-score and levels of obesity-related hormones, and that shared environmental factors also affect these endocrine traits in children.