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Pérusse, Louis

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Pérusse

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Louis

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Université Laval. Département de kinésiologie

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ncf10139306

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Voici les éléments 1 - 10 sur 22
  • PublicationRestreint
    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.
  • PublicationAccès 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.
  • PublicationRestreint
    Associations between glucose tolerance, insulin sensitivity and insulin secretion phenotypes and polymorphisms in adiponectin and adiponectin receptor genes in the Quebec Family Study
    (Wiley, 2008-02-19) Ruchat, Stéphanie-May; Loos, Ruth; Bouchard, Claude; Rankinen, Tuomo; Pérusse, Louis; Weisnagel, John; Vohl, Marie-Claude; Després, Jean-Pierre
    Aims:  Studies suggest that adiponectin (APM1) and its receptors 1 and 2 (AdipoR1 and AdipoR2) play an important role in the development of insulin resistance (IR). Our objective was to examine associations between APM1 (+45T>G, +276G>T and –3971A>G), AdipoR1 (−100G>T and −3882T>C) and AdipoR2 (−35361A>G and –1352G>A) genes single‐nucleotide polymorphisms (SNPs) and adiponectin plasma levels, indicators of glucose tolerance, insulin sensitivity (IS) and insulin secretion. Methods:  Six hundred and twenty‐two non‐diabetic subjects from the Quebec Family Study (QFS) underwent a 75‐g oral glucose tolerance test (OGTT), with measurement of fasting adiponectin, glucose, insulin and C‐peptide levels. Indices of glucose tolerance, IS and insulin secretion were derived from fasting and OGTT measurements. Results:  Significant evidence of association was found between indices of IS and APM1 and AdipoR1 SNPs. The APM1 –3971G/G homozygotes exhibited a reduced area under the curve of insulin during the OGTT (P = 0.007) and higher Cederholm index (P = 0.01) compared to the A/A homozygotes. The APM1 +45T>G variant was also associated with fasting (P = 0.002) and 2‐h (P = 0.007) glucose values as well as with higher Cederholm index (P = 0.04) and disposition index (P = 0.02). Finally, the AdipoR1 −3882T>C SNP was associated with fasting glucose (P = 0.03), the homeostasis model assessment for insulin resistance (P = 0.04) and an index of insulin secretion (P30/G30, P = 0.02). No evidence of association was found with plasma adiponectin levels. Conclusions:  These results provide evidence for an influence of common SNPs in the APM1 and AdipoR1 genes on different phenotypes of glucose and insulin metabolism associated with increased risk of type 2 diabetes.
  • PublicationRestreint
    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.
  • PublicationRestreint
    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.
  • PublicationAccès libre
    Genome-wide linkage scan reveals multiple susceptibility loci influencing lipid and lipoprotein levels in the Québec Family Study
    (American Society for Biochemistry et Molecular Biology, Inc., 2003-12-16) Bouchard, Claude; Chagnon, Yvon C.; Pérusse, Louis; Rice, Treva; Bossé, Yohan; Rao, D. C. (Dabeeru C.); Vohl, Marie-Claude; Després, Jean-Pierre
    A genome-wide linkage study was performed to identify chromosomal regions harboring genes influencing lipid and lipoprotein levels. Linkage analyses were conducted for four quantitative lipoprotein/lipid traits, i.e., total cholesterol, triglyceride, HDL-cholesterol (HDL-C), and LDL-C concentrations, in 930 subjects enrolled in the Québec Family Study. A maximum of 534 pairs of siblings from 292 nuclear families were available. Linkage was tested using both allele-sharing and variance-component linkage methods. The strongest evidence of linkage was found on chromosome 12q14.1 at marker D12S334 for HDL-C, with a logarithm of the odds (LOD) score of 4.06. Chromosomal regions harboring quantitative trait loci (QTLs) for LDL-C included 1q43 (LOD = 2.50), 11q23.2 (LOD = 3.22), 15q26.1 (LOD = 3.11), and 19q13.32 (LOD = 3.59). In the case of triglycerides, three markers located on 2p14, 11p13, and 11q24.1 provided suggestive evidence of linkage (LOD > 1.75). Tests for total cholesterol levels yielded significant evidence of linkage at 15q26.1 and 18q22.3 with the allele-sharing linkage method, but the results were nonsignificant with the variance-component method. In conclusion, this genome scan provides evidence for several QTLs influencing lipid and lipoprotein levels. Promising candidate genes were located in the vicinity of the genomic regions showing evidence of linkage.
  • PublicationRestreint
    Evidence for a major quantitative trait locus on chromosome 17q21 affecting low-density lipoprotein peak particle diameter
    (Grune & Stratton, 2003-05-05) Bouchard, Claude; Chagnon, Yvon C.; Pérusse, Louis; Lamarche, Benoît; Bossé, Yohan; Rice, Treva; Vohl, Marie-Claude; Rao, D. C. (Dabeeru C.); Després, Jean-Pierre
    Background— Several lines of evidence suggest that small dense LDL particles are associated with the risk of coronary heart disease. Heritability and segregation studies suggest that LDL particle size is characterized by a large genetic contribution and the presence of a putative major genetic locus. However, association and linkage analyses have thus far been inconclusive in identifying the underlying gene(s). Methods and Results— An autosomal genome-wide scan for LDL peak particle diameter (LDL-PPD) was performed in the Québec Family Study. A total of 442 markers were genotyped, with an average intermarker distance of 7.2 cM. LDL-PPD was measured by gradient gel electrophoresis in 681 subjects from 236 nuclear families. Linkage was tested by both sib-pair–based and variance components–based linkage methods. The strongest evidence of linkage was found on chromosome 17q21.33 at marker D17S1301, with an LOD score of 6.76 by the variance-components method for the phenotype adjusted for age, body mass index, and triglyceride levels. Similar results were obtained with the sib-pair method (P<0.0001). Other chromosomal regions harboring markers with highly suggestive evidence of linkage (P≤0.0023; LOD ≥1.75) include 1p31, 2q33.2, 4p15.2, 5q12.3, and 14q31. Several candidate genes are localized under the peak linkages, including apolipoprotein H on chromosome 17q, the apolipoprotein E receptor 2, and members of the phospholipase A2 family on chromosome 1p as well as HMG-CoA reductase on chromosome 5q. Conclusions— This genome-wide scan for LDL-PPD indicates the presence of a major quantitative trait locus located on chromosome 17q and others interesting loci influencing the phenotype.
  • PublicationRestreint
    Combined effects of PPARγ2 P12A and PPARα L162V polymorphisms on glucose and insulin homeostasis : the Québec Family Study
    (Springer-Verlag, 2003-11-20) Bouchard, Claude; Pérusse, Louis; Weisnagel, John; Bossé, Yohan; Vohl, Marie-Claude; Després, Jean-Pierre
    Peroxisome proliferator-activated receptors γ2 and α are nuclear factors known to be important regulators of lipid and glucose metabolism. Two polymorphisms, namely PPARγ2 P12A and PPARα L162V, were investigated for their individual and interaction effects on glucose and insulin homeostasis. Genotypes were determined in 663 nondiabetic adults participating in the Québec Family Study and who underwent an oral glucose tolerance test (OGTT). The insulin and C-peptide areas under the curve (AUC) following the OGTT were higher in subjects carrying the PPARα V162 allele compared to homozygous for the L162 allele. When subjects were grouped according to both polymorphisms, higher levels of insulin and C-peptide during the OGTT were observed for those carrying the PPARα V162 allele except when they carry at the same time the PPARγ2 A12 allele. Thus, the PPARγ2 A12 allele seems protective against the deleterious effect of the PPARα V162 allele. Furthermore, a significant gene-gene interaction was observed for the acute (0–30 min) (p<0.001) and the total (p=0.05) C-peptide AUC following the OGTT. These results provide evidence of a gene-gene interaction in the regulation of plasma glucose-insulin homeostasis, and emphasize that these interactions need to be taken into account when dissecting the genetic etiology of complex disorders.
  • PublicationRestreint
    Abdominal visceral fat is associated with a BclI restriction fragment length polymorphism at the glucocorticoid receptor gene locus
    (North American Association for the Study of Obesity, 1997-05-01) Buemann, Benjamin; Bouchard, Claude; Dionne, France T.; Chagnon, Monique; Chagnon, Yvon C.; Pérusse, Louis; Nadeau, André; Gagnon, Jacques; Tremblay, Angelo; Vohl, Marie-Claude; Després, Jean-Pierre
    Several investigations have suggested that body fat distribution is influenced by nonpathologic variations in the responsiveness to Cortisol. Genetic variations in the glucocorticoid receptor (GRL) could therefore potentially have an impact on the level of abdominal fat. A restriction fragment length polymorphism (RFLP) has previously been detected with the BelI restriction enzyme in the GRL gene identifying two alleles with fragment lengths of 4.5 and 2.3 kb. This study investigates whether abdominal fat areas measured by computerized tomography (CT) are associated with this polymorphism in 152 middle-aged men and women. The less frequent 4.5-kb allele was found to be associated with a higher abdominal visceral fat (A VF) area independently of total body fat mass (4.5/4.5 vs. 2.3/2.3 kb genotype; men: 190.7 ± 30.1 vs. 150.7 ± 33.3 cm2, p=0.04; women: 132.7 ± 37.3 vs. 101.3 ± 34.5 cm2, p=0.06). However, the association with AVF was seen only in subjects of the lower tertile of the percent body fat level. In these subjects, the polymorphism was found to account for 41% (p=0.003) and 35% (p=0.007), in men and women, respectively, of the total variance in AVF area. The consistent association between the GRL polymorphism detected with BelI and AVF area suggests that this gene or a locus in linkage disequilibrium with the BelI restriction site may contribute to the accumulation of AVF.
  • PublicationAccès libre
    Compendium of genome-wide scans of lipid-related phenotypes : adding a new genome-wide search of apolipoproteins levels
    (American Society for Biochemistry and Molecular Biology, 2004-09-16) Bouchard, Claude; Chagnon, Yvon C.; Pérusse, Louis; Rice, Treva; Bossé, Yohan; Rao, D. C.; Vohl, Marie-Claude; Després, Jean-Pierre
    The genetic dissection of complex inherited diseases is a major challenge. Despite limited success in finding genes, substantial data based on genome-wide scan strategies is now available for a variety of diseases and related phenotypes. This can perhaps best be appreciated in the field of lipid and lipoprotein levels, where the amount of information generated is becoming overwhelming. We have created a database containing the results from whole-genome scans of lipid-related phenotypes undertaken to date. The usefulness of this database is demonstrated by performing a new autosomal genomic scan on apolipoprotein B (apoB), LDL-apoB, and apoA-I levels, measured in 679 subjects of 243 nuclear families. Linkage was tested using both allele-sharing and variance-component methods. Only two loci provided support for linkage with both methods: a LDL-apoB locus on 18q21.32 and an apoA-I locus on 3p25.2. Adding those findings to the database highlighted the fact that the former is reported as a lipid-related locus for the first time, whereas the latter has been observed before. However, concerns arise when displaying all data on the same map, because a large portion of the genome is now covered with loci supported by at least suggestive evidence of linkage.