Peroxisome proliferator-activated receptor-gamma (PPARgamma) Pro12Ala polymorphism and risk for pediatric obesity.

BACKGROUND: Variation in the peroxisome-proliferator-activated receptor gamma (PPARgamma) gene has been reported to alter the risk for adiposity in adults. METHODS: We investigated the gender related association between the Pro12Ala variant (rs1801282) in obesity and insulin resistance traits in 794 peri-adolescent children aged 10-12 years of Greek origin from the Gene and Diet Attica Investigation (GENDAI) cohort. RESULTS: Gender stratified analysis suggested that in peri-adolescent boys, Ala carriers exhibited lower measures of skinfold (triceps: 16.9+/-6.9 vs. 19.4+/-7.9 mm, p=0.014; subscapular: 9.6+/-4.5 vs. 11.2+/-5.4 mm, p=0.016) and lower adiponectin concentrations (3.9+/-1.3 vs. 4.7+/-2.4 microg/mL, p=0.05). In peri-adolescent girls, Ala carriers had lower insulin concentrations (7.3+/-3.7 vs. 8.5+/-4.4 microU/mL, p=0.026) and lower values of homeostasis model assessment of insulin resistance (HOMA-IR) (1.5+/-0.8 vs. 1.8+/-0.96, p=0.019). Linear regression analysis revealed that the presence of the Ala allele in boys was a nominally significant predictor of obesity indices, including skin-folds (triceps: beta+/-SE: -2.3+/-1.1, p=0.032; subscapular: beta+/-SE: -2.3+/-1.1, p=0.04) and adiponectin concentrations (beta+/-SE: -0.7+/-0.4, p=0.05) after adjusting for potential covariates. In girls, the Ala allele was a predictor of insulin concentrations (beta+/-SE: -1.2+/-0.6, p=0.037) and HOMA-IR (beta+/-SE: -0.24+/-0.13, p=0.037). CONCLUSIONS: Our results suggest that adiposity in children is influenced by the Pro12Ala polymorphism in a gender specific manner.

The Gene-Diet Attica investigation on childhood obesity (GENDAI): overview of the study design.

BACKGROUND: There is limited evidence on the role of genetic and environmental factors in the etiology of childhood obesity, a major health problem worldwide. METHODS: The Gene-Diet Attica Investigation on childhood obesity (GENDAI) evaluates the contributions to and pivotal interactions of genetic, dietary and physical activity variables on children's weight. We describe the design, methodology, and present preliminary data. So far, 920 participants have been enrolled and the final projected sample is 1000 fifth- and sixth-grade students from selected elementary schools in Attica (10-14 years). In this school-based cross-sectional study, more than 400 variables describing anthropometric, dietary, clinical, genetic, sociodemographic and other lifestyle characteristics were collected from participating children and their families. RESULTS: Increased body mass index was identified in 39.3% of subjects (30.5% overweight and 8.8% obese), with males presenting a more unfavorable metabolic profile, i.e., higher blood lipids, glucose, and insulin, compared to females. Normal-weight children had a significant advantage when compared to all children of increased weight in terms of lipid profile and insulin, as well as behaviors examined. Specifically, normal-weight children exhibited less skipping of meals and less sedentary activities. CONCLUSIONS: The overall high prevalence of overweight and obesity in the current population is significant and underscores the need for environmental and genetic information that will shed light on the phenomenon of childhood obesity.

Association between TNF-alpha -308G>A polymorphism and the development of acute coronary syndromes in Greek subjects: the CARDIO2000-GENE Study.

PURPOSE: We investigated the association of a polymorphism within the promoter of TauNuF-alpha locus at the position -308 on the likelihood of having acute coronary syndromes (ACS) in Greek adults. METHODS: We studied demographic, lifestyle, and clinical information in 237 hospitalized patients (185 males) with a first event of an ACS and 237 matched by age and sex (controls) without any clinical evidence of coronary heart disease. Genotyping was performed by PCR-RFLP analysis. RESULTS: The genotype frequencies were in patients, 87% (n = 206), 12% (n = 29), and 1% (n = 2) for G/G, G/A, and A/A, and in controls, 96% (n = 227), 4% (n = 10), and 0% (n = 0) for G/G, G/A, and A/A, respectively (P = 0.04). After adjusting for age and sex, as well as various potential confounders, we observed that G/A or A/A genotypes were associated with 1.94-fold higher odds (95% CI 1.06 to 3.68) of ACS compared to G/G homozygotes. No gene to-gender or to-clinical syndrome interactions were observed. Further subgroup analysis showed that the distribution of TNF-alpha -308G>A polymorphism was associated with the presence of family history of CHD in patients, but not in controls. In particular, in G/A and A/A patients 17.2% reported family history of CHD, whereas in G/G patients, 34.5% reported family history (P = 0.036). CONCLUSIONS: Our findings may state a hypothesis of an association between the -308G>A TNF-alpha polymorphism the development of ACS and the presence of family history of CHD, in Greece.