Personne : Mauriege, Pascale
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Université Laval. Département de kinésiologie
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- PublicationRestreintPlasminogen-activator inhibitor-1 polymorphisms are associated with obesity and fat distribution in the Québec Family Study : evidence of interactions with menopause(Raven Press, 2005-01-01) Bouchard, Claude; Pérusse, Louis; Mauriege, Pascale; Vohl, Marie-Claude; Bouchard, LuigiObjective: Obesity is associated with increased plasma levels of plasminogen-activator inhibitor1 (PAI1), the major fibrinolysis inhibitor. PAI1 levels are also increased at menopause, a condition that is associated with fat mass gain, especially in the abdominal area. Design: We hypothesized that genetic variations within PAI1 gene are related to the amount of body fat and its regional distribution. We genotyped 666 subjects of the Que´bec Family Study for five PAI1 gene polymorphisms. Stratified analyses were performed with analysis of covariance in men (n = 280) and women (n = 386) separately. Results: PAI1-675 4G/5G polymorphism was strongly associated with body mass index (P # 0.01) and fat mass (P # 0.05) in women. The PAI1-675 4G/5G promoter polymorphism and the c.43G.A (p.A15T, rs6092) variant within the exon 1 were associated with abdominal visceral fat but only in postmenopausal women (P # 0.05). More specifically, homozygotes for the 2675 5G and the 43A alleles had about 50% more visceral fat compared to carriers of the 2675 4G allele as well as carriers of the 43G allele. No association was observed in men. Conclusion: Taken together, these results suggest that the PAI1 gene is associated with obesity and may modulate the changes in adipose tissue distribution generally observed at menopause.
- PublicationRestreintContribution of genetic and metabolic syndrome to omental adipose tissue PAI-1 gene mRNA and plasma levels in obesity(Springer Nature, 2010-02-02) Pérusse, Louis; Mauriege, Pascale; Lebel, Stéfane; Hould, Frédéric-Simon; Marceau, Picard; Vohl, Marie-Claude; Bouchard, Luigi; Bergeron, JeanBackground Plasminogen activator inhibitor type-1 (PAI-1) has already been associated with atherosclerosis; myocardial infarction; and cardiovascular disease risk factors such as obesity, insulin resistance, and dyslipidemia. However, factors regulating PAI-1 adipose tissue (AT) gene expression and plasma levels are not yet well defined. Aim This study aims to assess the contribution of PAI-1 omental AT mRNA levels and genetic and metabolic factors to variation in plasma PAI-1 concentrations. Methods Ninety-one non-diabetic premenopausal severely obese women (body mass index, BMI >35 kg/m2) undergoing bariatric surgery were phenotyped (fasting plasma glucose, lipid-lipoprotein, and PAI-1 levels) and genotyped for four PAI-1 polymorphisms. Omental AT PAI-1 mRNA levels were determined using real-time polymerase chain reaction. Stepwise regression analysis was used to identify independent PAI-1 AT mRNA and plasma level predictors. Results Among the variables included to the stepwise regression analysis, plasma high-density lipoprotein (HDL)-cholesterol (r = 0.38; p = 0.0004) and total cholesterol (r = 0.16; p = 0.0541) levels were the only two (out of 12) independent variables retained as predictive of PAI-1 omental AT mRNA levels, whereas BMI (r = 0.35; p = 0.0039), plasma HDL-cholesterol concentrations (r = −0.31; p = 0.0375), PAI-1 omental AT mRNA levels (r = 0.19; p = 0.0532) and PAI-1-844G/A (p = 0.0023), and rs6092 (p.A15T; p = 0.0358) polymorphisms contributed independently to plasma PAI-1 concentrations. Taken together, these variables explained 17.8% and 31.0% of the variability in PAI-1 AT mRNA and plasma levels, respectively. Conclusion These results suggest that PAI-1 polymorphisms contribute significantly to PAI-1 plasma levels but do not support the notion that omental AT is one of its major source.
- PublicationAccès libreImpact of adiponectin gene polymorphisms on plasma lipoprotein and adiponectin concentrations of viscerally obese men(Federation of American Societies for Experimental Biology, Lipid Research, 2004-11-16) Berthier, Marie-Thérèse; Côté, Mélanie.; Paradis, Ann-Marie; Mauriege, Pascale; Gaudet, Daniel; Houde, Alain; Vohl, Marie-Claude; Després, Jean-Pierre; Bergeron, JeanThe aim of this study was first to examine the relationships between adiponectin gene (Apm1) polymorphisms and anthropometric indices as well as plasma adiponectin and lipoprotein/lipid levels, and then to investigate whether the presence of visceral obesity or insulin resistance may modulate the impact of these polymorphisms on metabolic risk variables. Molecular screening of the Apm1 gene was achieved, and a sample of 270 unrelated men recruited from the greater Quebec City area and selected to cover a wide range of body fatness values was genotyped. Sequencing of the Apm1 gene revealed two previously reported polymorphisms (c.45T>G and c.276G>T) as well as two newly identified genetic variations (−13752delT and −13702G>C). Carriers of the c.276T allele had higher LDL-cholesterol and lower HDL-triglyceride concentrations than did 276G/G homozygotes (P = 0.02 and P = 0.01, respectively). Carriers of the c.45G allele exhibited higher plasma adiponectin concentrations than did 45T/T homozygotes (P = 0.04). After dividing each genotype group into subgroups for visceral AT, homozygotes for the normal allele at position −13752delT, carriers of the c.45G allele, and carriers of the c.276T allele had similar total apolipoprotein B (apoB) concentrations, whether they were viscerally obese or not. These results suggest that some Apm1 gene polymorphisms influence plasma adiponectin concentrations and lipoprotein/lipid levels. In addition, the impact of these polymorphisms is modulated by the presence of visceral obesity.