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Submitted on November 30, 2004
Accepted on April 5, 2005
USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030; Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio, Texas 78245
* To whom correspondence should be addressed. E-mail: nbutte{at}bcm.tmc.edu.
Context. Because of its anti-inflammatory and insulin-sensitizing properties, adiponectin may play a role in the development of cardiovascular disease (CVD) and type 2 diabetes (T2D).
Objectives. The aims of these analyses were 1) to estimate the heritability of fasting serum adiponectin; 2) to evaluate the effects of age, sex and body composition on fasting serum adiponectin; 3) to test for associations between fasting serum adiponectin and diet, fitness, energy expenditure and fat oxidation; and 4) to determine the relationships between fasting serum adiponectin, insulin and lipids, and blood pressure in Hispanic children.
Design. Genetic and environmental factors influencing fasting serum adiponectin were investigated in a cohort of children participating in the VIVA LA FAMILIA Study in 2000-2005.
Setting. Children's Nutrition Research Center
Participants. 805 Hispanic non-overweight and overweight children, ages 4-19 y
Main Measure. Fasting serum adiponectin
Result. Heritability (h2) of serum adiponectin was 0.93 ± 0.10 (P = 2.4 x 10-40). Adiponectin differed by age (P = 0.001), sex (P = 0.04) and weight status (P = 0.001). Adiponectin levels declined with age, in association with changes in sex hormones and growth factors. Adiponectin was not associated with macronutrient intake, fitness, 24-h energy expenditure, or fat oxidation. Controlling for age, sex and %fat mass, adiponectin was inversely associated with homeostasis model-insulin resistance (HOMA-IR), triglycerides/high-density lipoprotein cholesterol (TG/HDL-C), and systolic blood pressure (P = 0.001). Significant positive genetic correlations were detected between adiponectin and total cholesterol (
G =0.19), HDL-C (
G =0.32), low-density lipoprotein cholesterol (LDL-C) (
G =0.24), and insulin-like growth factor binding protein-1 (IGFBP-1) (
G =0.39), and negative genetic correlations between adiponectin and leptin (
G -0.30), TG (
G -0.21), TG/HDL-C (
G -0.33), and IGFBP-3 (
G -0.32), indicating shared genetic components in their expression.
Conclusion. The high heritability of adiponectin and pleiotropy seen between adiponectin and leptin, growth factors and lipids may play a role in the pathogenesis of CVD and T2D in overweight Hispanic children.
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