Personne :
Pérusse, Louis

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Structures organisationnelles
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Université Laval. Département de kinésiologie
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Voici les éléments 1 - 10 sur 101
  • Publication
    Plasminogen-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, Luigi
    Objective: 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.
  • Publication
    Prevalence and familial patterns of night eating in the Québec adipose and lifestyle investigation in youth (QUALITY) study
    (NAASO, the Obesity Society, 2012-03-19) Lundgren, Jennifer D.; Drapeau, Vicky; Gallant, Annette; Allison, Kelly C.; Pérusse, Louis; Tremblay, Angelo; Lemieux, Simone; Lambert, Marie; O’Loughlin, Jennifer; Stunkard, Albert J.
    The prevalence and familial patterns of night eating syndrome (NES) in families enrolled in the Québec Adipose and Lifestyle InvesTigation in Youth (QUALITY) study was examined. Families (n = 395; one child, mother, and father for whom at least one parent was obese or had abdominal obesity) completed the Night Eating Questionnaire (NEQ) as part of a longitudinal study on the development of metabolic disease in children at risk for obesity. Responses on the NEQ were used to establish a diagnosis of NES and to determine the correlation and heritability of NES symptoms in families. Using comprehensive research diagnostic criteria, full threshold NES was rare: 0% of children, 0.5% of mothers, and 0.3% of fathers met criteria. When controlling for age, sex, and BMI, NEQ scores of spouses were not significantly correlated, but mothers' NEQ scores were significantly correlated with the scores of both sons (r = 0.19, P < 0.001) and daughters (r = 0.15, P = 0.05). The heritability of NEQ scores was 0.24 when controlling for age, sex, and BMI. These findings replicate previous research suggesting a low prevalence of night eating behavior in children and the aggregation of NES in families.
  • Publication
    Influences of the phosphatidylcholine transfer protein gene variants on the LDL peak particle size
    (Elsevier, 2021-01-30) Bouchard, Claude; Berthier, Marie-Thérèse; Pérusse, Louis; Dolley, Guillaume; Lamarche, Benoît; Vohl, Marie-Claude; Després, Jean-Pierre
    Background: The small, dense LDL phenotype is associated with an increased cardiovascular disease risk. A genome-wide scan performed on 236 nuclear families of the Quebec Family Study (QFS) revealed a quantitative trait locus (QTL) affecting LDL peak particle size (LDL-PPD) and density on the 17q21 region. This region contains the phosphatidylcholine transfer protein gene (PCTP). In the liver, phosphatidylcholine transfer protein binds specifically phosphatidylcholine suggesting a role for this protein in the formation of HDL and possibly VLDL phospholipid membranes. Objectives: To test the association between two coding polymorphisms (c.29A>C (Glu10Ala) and c.188G>A (Cys63Tyr)) in PCTP gene and the LDL-PPD. Methods: LDL-PPD was measured by non-denaturating 2–16% polyacrylamide gradient gel electrophoresis on 623 QFS subjects. Results: After adjustment for age and sex, carriers of the c.29C allele showed larger LDL-PPD than A/A homozygotes (p < 0.05). These results remained significant when LDL-PPD was further adjusted for the effects of BMI and triglyceride levels (p < 0.04). We also observed a three-fold lower risk of having the small (LDL-PPD <256 Å), dense LDL phenotype in subjects carrying the c.29C allele, when compared to A/A homozygotes (OR = 0.35 (95% CI: 0.14–0.91; p = 0.03)). Conclusion: PCTP gene variants are associated with LDL-PPD.
  • Publication
    Differential methylation in visceral adipose tissue of obese men discordant for metabolic disturbances
    (American Physiological Society, 2014-03-15) Guénard, Frédéric; Biron, Simon; Biertho, Laurent; Pérusse, Louis; Lescelleur, Odette; Vohl, Marie-Claude; Deshaies, Yves; Marceau, Simon; Tchernof, André
    Obesity is associated with an increased risk of Type 2 diabetes and cardiovascular diseases (CVD). The severely obese population is heterogeneous regarding CVD risk profile. Our objective was to identify metabolic pathways potentially associated with development of metabolic syndrome (MetS) through an analysis of overrepresented pathways from differentially methylated genes between severely obese men with (MetS+) and without (MetS-) the MetS. Genome-wide quantitative DNA methylation analysis in VAT of severely obese men was carried out using the Infinium HumanMethylation450 BeadChip. Differences in methylation levels between MetS+ (n = 7) and MetS- (n = 7) groups were tested. Overrepresented pathways from the list of differentially methylated genes were identified and visualized with the Ingenuity Pathway Analysis system. Differential methylation analysis between MetS+ and MetS- groups identified 8,578 methylation probes (3,258 annotated genes) with significant differences in methylation levels (false discovery rate-corrected DiffScore ≥ |13| ∼ P ≤ 0.05). Pathway analysis from differentially methylated genes identified 41 overrepresented (P ≤ 0.05) pathways. The most overrepresented pathways were related to structural components of the cell membrane, inflammation and immunity and cell cycle regulation. This study provides potential targets associated with adipose tissue dysfunction and development of the MetS.
  • Publication
    Effect of implementation intentions to change behaviour : moderation by intention stability
    (Sage Publications, Inc., 2010-02-01) Bélanger-Gravel, Ariane; Pérusse, Louis; Godin, Gaston; Amireault, Steve; Gallani, Maria Cecilia; Vohl, Marie-Claude
    The aim of this study was to assess the effects of implementation intentions on leisure-time physical activity, taking into account the stability of intention. At baseline (T0), 349 participants completed a psychosocial questionnaire and were randomly assigned to implementation intention or control condition. Three months after baseline assessment (T1), participants in the experimental group were asked to plan where, when, and how they would exercise. Leisure-time physical activity was assessed 3 mo. later (i.e., at 6-mo. follow-up; T2). The intervention had no significant effect on physical activity at 6-mo. follow-up. However, a significant interaction of group and intention stability was observed, with the effect of the intervention on behaviour statistically significant only among those with unstable intention. Intention stability thus moderated the effect of the intervention, i.e., the intervention was more successful among individuals who needed support to change (unstable intenders).
  • Publication
    A variant in the LRRFIP1 gene is associated with adiposity and inflammation
    (NAASO the Obesity Society, 2013-03-16) Bouchard, Claude; Plourde, Mélanie.; Bellis, Claire; Marette, André; Carless, Melanie; Pérusse, Louis; Dyer, Thomas; Dolley, Guillaume; Vohl, Marie-Claude; Després, Jean-Pierre; Blangero, John
    Inflammation is an important factor linking abdominal obesity with insulin resistance and related cardiometabolic risk. A genome-wide association study of adiposity-related traits performed in the Quebec Family Study (QFS) revealed that a single-nucleotide polymorphism (SNP) in the LRRFIP1 gene (rs11680012) was associated with abdominal adiposity (P = 4.6 × 10–6). Objective: The objective of this study was to assess the relationship between polymorphisms in LRRFIP1 gene and adiposity (BMI, fat mass (FM), waist circumference (WC), and computed tomography-derived areas of total, subcutaneous and visceral abdominal adipose tissue) and markers of inflammation (C-reactive protein (CRP) and interleukin-6 (IL-6)). Design and Methods: Using Sequenom, 16 tag SNPs in the LRRFIP1 gene, capturing 78% of the genetic variation, were genotyped in 926 participants of the QFS. Results: Eight SNPs (rs7575941, rs3769053, rs11689421, rs3820808, rs11680012, rs3806505, rs6739130, and rs11686141) showed evidence of association with at least two adiposity phenotypes and plasma levels of one marker of inflammation. The strongest evidence of association was observed with rs11680012, which explained 1.8–3.4% of the variance in areas of abdominal adiposity and 2.0% of the variation in CRP levels. Carriers of the rare allele of rs11680012 had ∼30% more abdominal adiposity (P values between 2.7 × 10–4 and 3.8 × 10–6) and 75% higher CRP levels (P = 1.6 × 10–4) than the common allele in age and sex adjusted data. Rs11680012 is a G/C SNP converting an arginine into a threonine and this amino acid substitution may potentially alter exonic splicing. Conclusion: This gene may therefore represent a potential interesting target to investigate in further functional studies on adiposity and inflammation.
  • Publication
    Accès libre
    The T111I mutation in the EL gene modulates the impact of dietary fat on the HDL profile in women
    (American Society for Biochemistry and Molecular Biology, 2003-07-16) Bouchard, Claude; Pérusse, Louis; Lamarche, Benoît; Bossé, Yohan; Paradis, Marie-Ève; Vohl, Marie-Claude; Després, Jean-Pierre; Couture, Patrick
    The objective of the present study was to examine the impact of the T111I missense mutation in exon 3 of the endothelial lipase (EL) gene on HDL and its potential interaction effect with dietary fat. The study sample included 281 women and 216 men aged between 17 and 76 years from the Québec Family Study. Plasma HDL3-C levels of I111I homozygote women were higher compared with those of women carrying the wild-type allele (P 0.03). These differences were not attenuated when adjusted for levels of obesity and were not observed among men. Dietary PUFA interacted with the T111I mutation to modulate apolipoprotein A-I (apoA-I) and HDL3-C levels among women. Specifically, a diet rich in PUFA was associated with increased apoA-I levels among women carriers of the I111 allele and with decreased apoA-I among women homozygotes for the wild-type allele (P 0.002). A similar interaction was observed with plasma HDL3-C levels (P 0.003). These interactions were not observed among men. In conclusion, the EL T111I mutation appears to have a modest effect on plasma HDL levels. The gene-diet interaction among women, however, suggests that the T111I missense mutation may confer protection against the lowering effect of a high dietary PUFA intake on plasma apoA-I and HDL3-C levels.—Paradis, M-E., P. Couture, Y. Bossé, J-P. Després, L. Pérusse, C. Bouchard, M-C. Vohl, and B. Lamarche. The T111I mutation in the EL gene modulates the impact of dietary fat on the HDL profile in women.
  • Publication
    Association between micro-opioid receptor-1 102T>C polymorphism and intermediate type 2 diabetes phenotypes : results from the Quebec Family Study (QFS)
    (Australian Society for Medical Research, 2008-08-01) Ruchat, Stéphanie-May; Girard, Martine; Bouchard, Claude; Pérusse, Louis; Weisnagel, John; Vohl, Marie-Claude
    It has been suggested recently that molecules expressed both in the pancreas and hypothalamus, such as mu-opioid receptor 1 (OPRM1), could form an integrated brain-liver system, which may sense glucose levels and therefore contribute to the development of type 2 diabetes mellitus (T2DM). In the present study, we tested associations between OPRM1 gene polymorphisms (rs1799971, 102T/C and rs0648007G/A) and indices of glucose tolerance, insulin sensitivity (IS) and insulin secretion derived from plasma measures obtained in a fasting state and following a 75 g oral glucose tolerance test (OGTT) in 749 subjects from the Quebec Family Study (QFS). Polymorphisms were tested for association with glucose tolerance (normal vs IFG and T2DM combined) by calculating a chi(2) statistic and corresponding P values, whereas associations with quantitative measures of glucose tolerance, IS and insulin secretion were tested using mixed linear models implemented in the MIXED procedure of sas (SAS Institute, Cary, NC, USA). Associations were found between 102T/C OPRM1 and indices of glucose tolerance and IS. Compared with T/T homozygotes, carriers of the OPRM1 C-102 variant exhibited a better glucose tolerance with a lower (P = 0.006) glucose area under the curve (AUC) following the OGTT and a better IS with a higher (P = 0.03) value of the Cederholm index, a numerical index of the curve relating glucose uptake to the log(10) plasma insulin levels during the OGTT. The results of the present study reveal that the 102T/C OPRM1 gene polymorphism is associated with a better glucose tolerance and improved IS, both of which suggest a potential protective effect of this variant on T2DM risk.
  • Publication
    Accès libre
    Genome-wide meta-analysis of 241,258 adults accounting for smoking behaviour identifies novel loci for obesity traits
    (Nature Publishing Group, 2017-04-26) Justice, Anne E.; Pérusse, Louis; Vohl, Marie-Claude; Cupples, L. Adrienne
    Few genome-wide association studies (GWAS) account for environmental exposures, like smoking, potentially impacting the overall trait variance when investigating the genetic contribution to obesity-related traits. Here, we use GWAS data from 51,080 current smokers and 190,178 nonsmokers (87% European descent) to identify loci influencing BMI and central adiposity, measured as waist circumference and waist-to-hip ratio both adjusted for BMI. We identify 23 novel genetic loci, and 9 loci with convincing evidence of gene-smoking interaction (GxSMK) on obesity-related traits. We show consistent direction of effect for all identified loci and significance for 18 novel and for 5 interaction loci in an independent study sample. These loci highlight novel biological functions, including response to oxidative stress, addictive behaviour, and regulatory functions emphasizing the importance of accounting for environment in genetic analyses. Our results suggest that tobacco smoking may alter the genetic susceptibility to overall adiposity and body fat distribution.
  • Publication
    Accès libre
    Familial resemblances in blood leukocyte DNA methylation levels
    (Landes Bioscience, 2016-11-01) Pérusse, Louis; Guénard, Frédéric; Lamarche, Benoît; Tremblay, Bénédicte L.; Vohl, Marie-Claude
    Epigenetic factors such as DNA methylation are DNA alterations affecting gene expression that can convey environmental information through generations. Only a few studies have demonstrated epigenetic inheritance in humans. Our objective is to quantify genetic and common environmental determinants of familial resemblances in DNA methylation levels, using a family based sample. DNA methylation was measured in 48 French Canadians from 16 families as part of the GENERATION Study. We used the Illumina HumanMethylation450 BeadChip array to measure DNA methylation levels in blood leukocytes on 485,577 CpG sites. Heritability was assessed using the variance components method implemented in the QTDT software, which partitions the variance into polygenic (G), common environmental (C), and non-shared environmental (E) effects. We computed maximal heritability, genetic heritability, and common environmental effect for all probes (12.7%, 8.2%, and 4.5%, respectively) and for statistically significant probes (81.8%, 26.9%, and 54.9%, respectively). Higher maximal heritability was observed in the Major Histocompatibility Complex region on chromosome 6. In conclusion, familial resemblances in DNA methylation levels are mainly attributable to genetic factors when considering the average across the genome, but common environmental effect plays an important role when considering statistically significant probes. Further epigenome-wide studies on larger samples combined with genome-wide genotyping studies are needed to better understand the underlying mechanisms of DNA methylation heritability.