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Bouchard, Claude

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Bouchard
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Claude
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Département d'éducation physique, Faculté des sciences de l'éducation, Université Laval
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Voici les éléments 1 - 10 sur 48
  • Publication
    Restreint
    Long-term adiposity changes are related to a glucocorticoid receptor polymorphism in young females
    (Oxford Academic, 2003-07-01) Drapeau, Vicky; Bouchard, Claude; Pérusse, Louis; Tremblay, Angelo; Bouchard, Luigi; Després, Jean-Pierre
    Male and female preadolescents and adolescents who participated in phase 1 of the Québec Family Study, and who were retested about 12 yr later, were recruited and subdivided on the basis of a genetic variant within the intron 2 of the glucocorticoid receptor (GRL IVS2-BclI). The increase in sc adiposity over the 12-yr follow-up period in the 4.5/2.3 genotype female subgroup was more than twice that observed in the 4.5/4.5 and the 2.3/2.3 genotype subgroups (P < 0.01). The statistical significance of this difference was essentially unchanged after adjusting for changes, over time, in percent dietary energy as fat, alcohol consumption, and participation in vigorous physical activity. In male subjects, the same trend was found, but it did not reach statistical significance. In conclusion, this study suggests that a significant interaction effect exists between variation in the glucocorticoid receptor gene and body fat gain in female subjects experiencing the transition between adolescence and adulthood. Further research will, however, be necessary to characterize the lifestyle factors promoting fat accumulation, over time, among genetically susceptible individuals.
  • Publication
    Restreint
    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
    Restreint
    Evidence of a quantitative trait locus for energy and macronutrient intake on chromosome 3q27.3 in the Quebec Family Study
    (American Society for Clinical Nutrition, 2008-10-01) Choquette, Anne.; Bouchard, Claude; Chagnon, Yvon C.; Pérusse, Louis; Tremblay, Angelo; Lemieux, Simone; Vohl, Marie-Claude
    Background: Little is known about the genes influencing dietary energy and nutrient intakes, despite evidence that these intakes are influenced by genetic factors. Objective: We aimed to identify, by using a genome-wide linkage analysis, chromosomal regions harboring genes that affect energy and macronutrient intakes. Design: Energy, carbohydrate, lipid, and protein intakes were assessed in 836 subjects from 217 families by using a 3-d dietary record. A total of 443 markers were genotyped and tested for linkage; age- and sex-adjusted energy and macronutrient intakes were expressed in grams and as percentages of total energy intake. Regression-based (Haseman-Elston) and variance-component (MERLIN) methods were applied to test for linkage with dietary data. A maximum of 454 sibpairs from 217 nuclear families were available for analysis. Results: The genome scan provided suggestive evidence (P 0.0023) for the presence of 6 quantitative trait linkages influencing total caloric and macronutrient intakes in the Québec Family Study. Of these, multiple linkages were found on chromosome 3q27.3, in a region harboring the adiponectin gene, at marker D3S1262 for energy [logarithm of odds (LOD): 2.24], carbohydrate (LOD: 2.00), and lipid (LOD: 1.65) intakes. The peak linkages for carbohydrate, lipid, and proteinintakes were found on chromosomes 1p32.2 (LOD: 2.39), 1p35.2 (LOD: 2.41), and 10p15.3 (LOD: 2.72), respectively. The linkage results remained significant after adjustment for body mass index, which suggested that the genes underlying these quantitative trait linkages influence dietary intake independent of body size. Conclusion: The linkage on chromosome 3q27.3 with energy, lipid, and carbohydrate intakes suggests that this region of the genome may harbor genes that influence energy and macronutrient intakes in humans.
  • Publication
    Restreint
    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
    Restreint
    Associations between USF1 gene variants and cardiovascular risk factors in the Quebec Family Study
    (Munksgaard, 2007-01-22) Choquette, Anne.; Bouchard, Claude; Pérusse, Louis; Houde, Alain; Vohl, Marie-Claude; Bouchard, Luigi
    Cardiovascular (CVD) risk factors are under the influence of environmental and genetic factors. Human upstream transcription factor 1 gene (USF1) encodes for a transcription factor, which modulates the expression of genes involved in lipid and carbohydrate metabolic pathways. The aim of this study was to test the hypothesis that USF1 gene variants are associated with CVD risk factors in the Quebec Family Study (QFS). USF1 has been sequenced in 20 QFS subjects with high plasma apolipoprotein B100 (APOB) levels (>1.14 g/l) and small, dense low‐density lipoprotein (LDL) particles (≥250.7 Å and ≤255.9 Å), as well as in five subjects with larger LDL particles. Ten variants were identified in non‐coding regions of USF1. Two of these polymorphisms (intron 7 c.561–100 G>A, and exon 11 c.*187 C>T) as well as the c.‐56 A>G polymorphism, were genotyped and analyzed in 760 subjects from QFS. Association studies showed that women with c.561‐100 A/A and c.*187 T/T genotypes had more favorable adiposity indices (<0.04). In summary, significant associations between relatively common USF1 genetic variants and CVD risk factors were observed in French Canadians.
  • Publication
    Restreint
    Apolipoprotein B-100 gene EcoRI polymorphism : relations to the plasma lipoprotein changes associated with abdominal visceral obesity
    (American Heart Association, 1994-04-01) Bouchard, Claude; Pouliot, Marie-Christine; Dionne, France T.; Lupien, Paul-J.; Moorjani, Sital; Prud'homme, Denis; Vohl, Marie-Claude; Després, Jean-Pierre
    The aim of this study was to investigate whether the EcoRI restriction fragment length polymorphism (RFLP) of the apolipoprotein (apo) B-100 gene influences the associations described among obesity, regional adipose tissue distribution, and plasma lipoprotein levels. For this purpose, blood samples were collected from 56 healthy men for whom we had extensive measurements of regional adipose tissue distribution (both anthropometric and computed tomography-derived measurements) and data on the plasma lipoprotein-lipid profile. DNA was extracted from white blood cells, and RFLP analysis was performed. Subjects were classified into two groups on the basis of their apoB-100 EcoRI genotype: subjects homozygous for the major 11-kb allele, the 11/11 group (n = 40), and subjects carrying the minor 13-kb allele, the 13/11 group (n = 16). Subjects carrying the 13-kb allele had lower percent body fat and abdominal adipose tissue accumulation than subjects homozygous for the 11-kb allele (P < .05). Although leaner, the 13/11 group did not show a more favorable plasma lipoprotein-lipid profile than the group homozygous for the 11-kb allele. In fact, after statistical control for the difference in percent body fat between the two genotype groups, the 13/11 group showed significantly higher plasma cholesterol levels (P < .05) and nearly significantly higher apoB levels than the 11/11 group (P = .06). The association patterns between indices of regional adiposity and plasma cholesterol and apoB levels were also different between the two EcoRI genotype groups. Only in the 13/11 group was the abdominal visceral adipose tissue area significantly associated with these plasma variables.
  • Publication
    Restreint
    GAD2 gene sequence variations are associated with eating behaviors and weight gain in women from the Quebec family study
    (Pergamon Press, 2009-08-15) Drapeau, Vicky; Choquette, Anne.; Bouchard, Claude; Pérusse, Louis; Tremblay, Angelo; Lemieux, Simone; Vohl, Marie-Claude
    The glutamate decarboxylase 2 (GAD2) gene encodes for the glutamic acid decarboxylase enzyme (GAD65), which is implicated in the formation of the γ-aminobutyric acid (GABA), a neurotransmitter involved in the regulation of food intake. The objective of the present study was to test for association between GAD2 singlenucleotide polymorphisms (SNPs) and eating behaviors, dietary intake and obesity in subjects (n= 873) from the Quebec Family Study (QFS). Energy and macronutrient intakes were measured using a 3-day dietary record and eating behaviors were assessed using the Three-Factor Eating Questionnaire (TFEQ). Six SNPs capturing about 90% of GAD2 gene variability were genotyped and tested for association with age- and BMI- adjusted phenotypes. No evidence of association was found in men. In women, a SNP (rs992990; c.61450 C>A) was associated with disinhibition (p= 0.028), emotional susceptibility to disinhibition (p= 0.0005) and susceptibility to hunger (p= 0.028). Another SNP (rs7908975; c.8473A>C) was associated with carbohydrate (p= 0.021) and lipid (p= 0.021) intakes, disinhibition (p= 0.011) and two of its subscales (emotional and situational susceptibility) as well as with avoidance of fattening foods (p= 0.036). Six-year weight gain was two times higher in women carrying the variants associated with eating behaviors: 4.2 kg (vs 2.1 kg in non-carriers) in A-allele carriers of c.61450 C>A (p= 0.038) and 4.9 kg (vs 2.5 kg in noncarriers) in C-allele carriers of c. 8473 A>C (p= 0.013). The results suggest a role for the GAD2 gene in determining food intake, eating behaviors and weight gain over time in women.
  • Publication
    Restreint
    Parental eating behavior traits are related to offspring BMI in the Québec Family Study
    (Newman Pub., 2013-02-12) Drapeau, Vicky; Bouchard, Claude; Gallant, Annette; Pérusse, Louis; Tremblay, Angelo; Després, Jean-Pierre
    Objective: Parental eating behavior traits have been shown to be related to the adiposity of their young children. It is unknown whether this relationship persists in older offspring or whether rigid or flexible control are involved. The objective of this study was to test the hypothesis that parental eating behavior traits, as measured by the Three-Factor Eating Questionnaire (TFEQ), are related to offspring body weight. Methods: Cross-sectional anthropometric and TFEQ data from phase 2 and 3 of the Québec Family Study generated 192 parent–offspring dyads (offspring age range: 10–37 years). Relationships were adjusted for offspring age, sex and reported physical activity, number of offspring per family and parent body mass index (BMI). Results: In all parent–offspring dyads, parental rigid control and disinhibition scores were positively related to offspring BMI (r=0.17, P=0.02; r=0.18, P<0.01, respectively). There were no significant relationships between cognitive restraint (P=0.75) or flexible control (P=0.06) with offspring BMI. Regression models revealed that parent disinhibition mediated the relationship between parent and offspring BMI, whereas rigid control of the parent moderated this relationship. The interaction effect between parental rigid control and disinhibition was a significant predictor of offspring BMI (β=0.13, P=0.05). Conclusion: Family environmental factors, such as parental eating behavior traits, are related to BMI of older offspring, and should be a focus in the prevention of obesity transmission within families.
  • Publication
    Accès libre
    The three-factor eating questionnaire and BMI in adolescents : results from the Quebec Family Study
    (Cambridge, 2010-05-07) Drapeau, Vicky; Bouchard, Claude; Gallant, Annette; Pérusse, Louis; Tremblay, Angelo; Després, Jean-Pierre
    Eating behaviour traits are associated with body weight variations in adults. The Three-Factor Eating Questionnaire (TFEQ) measures cognitive restraint, disinhibition and hunger, as well as their corresponding subscales, e.g. rigid and flexible control. The TFEQ has not been widely used in adolescents to investigate eating behaviour traits associated with body weight. The aim of the present study was to assess whether eating behaviour traits were associated with BMI in male and female adolescents. Sixty adolescents (thirty females and thirty males; mean age 15·0 (sd 2·4) years) from the Québec Family Study completed the TFEQ and 3 d dietary records. There were no sex differences in the TFEQ scores. Rigid control, disinhibition and emotional susceptibility (to overeat) were positively related to BMI z-scores for the entire sample (r 0·3, P < 0·05). There was a positive relationship between BMI z-scores and rigid control (r 0·39, P < 0·05) in females, while BMI z-scores were positively related to emotional susceptibility (r 0·42, P < 0·02) and disinhibition (r 0·41, P < 0·03) in males. Adolescents characterised by both high disinhibition and high rigid control had significantly higher BMI z-scores than those by both low disinhibition and low rigid control. There were no significant differences in BMI z-scores between the flexible control categories. Dietary macronutrient content was not consistently related to eating behaviour traits. These results show that the eating behaviour traits of disinhibition and rigid control are independently related to BMI z-scores in this group of adolescents.
  • Publication
    Restreint
    Heritability of LDL peak particle diameter in the Quebec Family Study
    (Wiley-Liss, Inc., 2003-11-18) Bouchard, Claude; Pérusse, Louis; Lamarche, Benoît; Bossé, Yohan; Rice, Treva; Vohl, Marie-Claude; Rao, D. C. (Dabeeru C.); Després, Jean-Pierre
    LDL size has been associated with the risk of coronary heart disease. The objective of the present study was to verify whether familial factors influence LDL peak particle diameter (LDL‐PPD), a quantitative trait reflecting the size of the major LDL subclass. LDL‐PPD was measured by 2–16% polyacrylamide gradient gel electrophoresis in 681 members of 236 nuclear families participating in the Quebec Family Study. LDL‐PPD was adjusted for age (LDL‐PPD1), age and body mass index (LDL‐PPD2), or age, body mass index, and plasma triglyceride levels (LDL‐PPD3) separately in men and women. The residual scores were used to test for familial aggregation, using an ANOVA and to compute maximum likelihood estimates of familial correlations. The ANOVA test revealed that family lines accounted for 47.4%, 46.7%, and 48.9% of the variance in the LDL‐PPD1, LDL‐PPD2, and LDL‐PPD3 phenotypes, respectively. The pattern of familial correlations revealed no significant spouse correlations but significant parent‐offspring and sibling correlations for the three LDL‐PPD phenotypes, with maximal heritability estimates of 59%, 58%, and 52% for LDL‐PPD1, LDL‐PPD2, and LDL‐PPD3, respectively. These results suggest that LDL‐PPD strongly aggregates in families, and that the familial resemblance appears to be primarily attributable to genetic factors. Genes responsible for this genetic contribution remain to be identified. Genet Epidemiol 25:375–381, 2003. © 2003 Wiley‐Liss, Inc.