Contribution of genetic and metabolic syndrome to omental adipose tissue PAI-1 gene mRNA and plasma levels in obesity

DC FieldValueLanguage
dc.contributor.authorBouchard, Luigi-
dc.contributor.authorVohl, Marie-Claude-
dc.contributor.authorLebel, Stéfane-
dc.contributor.authorHould, Frédéric-Simon-
dc.contributor.authorMarceau, Picard-
dc.contributor.authorBergeron, Jean-
dc.contributor.authorPérusse, Louis-
dc.contributor.authorMauriege, Pascale-
dc.date.accessioned2020-07-31T16:36:12Z-
dc.date.available9999-12-31-
dc.date.issued2010-02-02-
dc.identifier.issn0960-8923fr
dc.identifier.urihttp://hdl.handle.net/20.500.11794/39938-
dc.description.abstractBackground 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.fr
dc.languageengfr
dc.publisherSpringer Naturefr
dc.subjectMetabolic syndromefr
dc.subjectAbdominal obesityfr
dc.subjectGene expression regulationfr
dc.subjectAdipose tissuefr
dc.titleContribution of genetic and metabolic syndrome to omental adipose tissue PAI-1 gene mRNA and plasma levels in obesityfr
dc.typeCOAR1_1::Texte::Périodique::Revue::Contribution à un journal::Article::Article de recherchefr
dcterms.bibliographicCitationObesity Surgery, Vol. 20 (4), 492–499 (2010)fr
dc.identifier.doi10.1007/s11695-010-0079-1fr
dc.subject.rvmSyndrome métaboliquefr
dc.subject.rvmObésité androïdefr
dc.subject.rvmTissu adipeuxfr
dc.subject.rvmExpression géniquefr
dc.subject.rvmDosage plasmatiquefr
rioxxterms.versionVersion of Recordfr
rioxxterms.version_of_recordhttp://dx.doi.org/10.1007/s11695-010-0079-1fr
rioxxterms.project.funder_nameMerck Frosstfr
rioxxterms.project.funder_nameUniversité Lavalfr
rioxxterms.project.funder_nameCanadian Institutes of Health Researchfr
bul.rights.periodeEmbargoInfinifr
Collection:Articles publiés dans des revues avec comité de lecture

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