Obesity, a highly prevalent condition, is heterogeneous with regard to its impact on cardiovascular disease (CVD) risk. Epidemiological observations and metabolic investigations have consistently demonstrated that the accumulation of excess visceral fat is related to an increased risk of CVD as well as several metabolic and inflammatory perturbations. In the past decade, data from several studies have served to emphasize that atherosclerosis has an inflammatory component that may contribute to several key pathophysiological processes. Study data have also highlighted the finding that the expanded visceral fat is infiltrated by macrophages that conduct "cross-talk" with adipose tissue through several significant mechanisms. In this review, we provide, in the context of CVD risk, an up-to-date account of the complex interactions that occur between a dysfunctional adipose tissue phenotype and inflammation.
The metabolic syndrome is a complex disorder characterized by an atherogenic dyslipidemia resulting from the interaction between genetic and nutritional factors. The objective of this study was to examine in a cohort of 720 adults participating in the Québec Family Study (QFS) whether dietary fat interacts with the P12A polymorphism in the gene encoding the peroxisome proliferator-activated receptor-gamma (PPAR-gamma), a nuclear factor that regulates lipid and glucose homeostasis. Carriers of the A12 allele had a higher body mass index (BMI), waist circumference, fat mass as well as subcutaneous adipose tissue and visceral adipose tissue (VAT) areas both assessed by computed tomography than P12/P12 homozygotes. Total fat and saturated fat intakes estimated from a 3-day food record were significantly correlated with several components of the metabolic syndrome in P12/P12 homozygotes. None of these expected associations were observed among carriers of the A12 allele. Furthermore, in a model including the PPAR-gamma P12A polymorphism, fat intake, age and gender, PPAR-gamma P12A and its interaction with fat intake were associated with BMI and waist circumference. Similar results were obtained when saturated fat intake replaced total fat intake into the model. When the two genotype groups were further classified into quartiles of total fat or saturated fat intake and their characteristics compared, an increase in fat intake was associated with an increase in waist circumference in P12/P12 homozygotes but not in A12 carriers. There was no difference in the waist circumference in carriers of the A12 allele whether the fat or the saturated fat intake was high or low. These results suggest that the PPAR-gamma P12A polymorphism can modulate the association between dietary fat intake and components of the metabolic syndrome.
PURPOSE:The purpose of this study was to examine the association of body mass index (BMI) and aerobic fitness on cardiovascular disease (CVD) risk factors in adolescents. METHODS: The sample included 416 boys and 345 girls 9-18 y of age from the Québec Family Study. Participants were crosstabulated into four groups using a median split of age-adjusted physical working capacity (PWC) and body mass index (BMI). Group differences in age-adjusted CVD risk factors (blood pressures, fasting total cholesterol (CHOL), LDL -C, HDL-C, HDL/ CHOL, triglycerides, glucose, and a composite risk factor score) were examined by two-way ANOVA. RESULTS: Several CVD risk factors showed significant main effects for PWC, BMI and/or the PWC by BMI interaction. In general, low fit males and females had higher blood lipids and glucose compared to their high fit counterparts within BMI categories although none of the differences reached statistical significance. The high fit/low BMI group showed the best CVD risk factor profile while the low fit/high BMI showed a poorer profile as evidenced by several significant differences between these two groups. Other significant differences occurred for various risk factors between groups. CONCLUSION: Both aerobic fitness and BMI show an independent association with CVD risk factors in adolescents.
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