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Bouchard, Claude

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Bouchard

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Claude

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Université Laval. Département de kinésiologie

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ncf10057564

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Voici les éléments 1 - 10 sur 27
  • 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.
  • 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.
  • 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
    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 gamma-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 single-nucleotide 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: 4.2kg (vs 2.1kg in non-carriers) in A-allele carriers of c.61450 C>A (p=0.038) and 4.9kg (vs 2.5kg in non-carriers) 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.
  • 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
    Modifications in food-group consumption are related to long-term body-weight changes
    (Journal of Clinical Nutrition, 2004-07-01) Drapeau, Vicky; Bouchard, Claude; Leblanc, Claude.; Fournier, Guy; Tremblay, Angelo; Allard, Lucie; Després, Jean-Pierre
    Background: Dietary patterns play an important role in the control of body weight. Objective: The aim of this study was to verify whether changes in some dietary patterns over a 6-y follow-up period would be associated with weight changes. Design: A sample of 248 volunteers of the Québec Family Study were measured twice (visit 1: 1989–1994; visit 2: 1995–2000). Body weight, percentage body fat, subcutaneous skinfold thicknesses, and waist circumference measurements as well as 3-d dietary and physical activity records were obtained at each visit. At visit 2, all participants filled out a food-based questionnaire examining changes in the consumption of 10 food categories. To further investigate the relation between changes in food-group consumption and bodyweight changes, a total of 51 food subcategories were identified from dietary records. Results: A self-reported decrease in the consumption of food in the fat group or an increase in consumption in the fruit group from the food-based questionnaire predicted a lower increase in body weight and adiposity indicators over time. A more detailed examination of the change in food groups between diet records revealed that increases in the consumption of whole fruit as well as skimmed milk and partly skimmed milk were the 2 food patterns that negatively correlated with the changes of each body weight–related indicator. Conclusions:These results show that changes in the consumption of some specific food groups are associated with body-weight changes. Such specific eating patterns could help to improve obesity treatment and prevention.
  • PublicationRestreint
    Genetic variants of FTO influence adiposity, insulin sensitivity, leptin levels, and resting metabolic rate in the Quebec family study
    (American Diabetes Association, 2008-03-03) Do, Ron; Bouchard, Claude; Bailey, Swneke D.; Pérusse, Louis; Desbiens, Katia; Vohl, Marie-Claude; Belisle, Alexandre; Montpetit, Alexandre; Engert, James
    Objective: A genome-wide association study conducted by the Wellcome Trust Case Control Consortium recently associated single nucleotide polymorphisms (SNPs) in the FTO (fatso/fat mass and obesity associated) gene with type 2 diabetes. These associations were shown to be mediated by obesity. Other research groups found similar results in Europeans and Hispanics but not African Americans. The mechanism by which FTO influences obesity and type 2 diabetes is currently unknown. The present study investigated the role of two FTO SNPs (rs17817449 and rs1421085) in adiposity, insulin sensitivity, and body weight regulation, including energy intake and expenditure. Research design and methods: We genotyped 908 individuals from the Quebec City metropolitan area that participated in the Quebec Family Study, a long-term study of extensively phenotyped individuals designed to investigate factors involved in adiposity. Results: We found significant associations for both SNPs with several obesity-related phenotypes. In particular, rs17817449 was associated with BMI (P = 0.0014), weight (P = 0.0059), and waist circumference (P = 0.0021) under an additive model. In addition, this FTO SNP influenced fasting insulin (P = 0.011), homeostasis model assessment of insulin resistance (P = 0.038), and an insulin sensitivity index derived from an oral glucose tolerance test (P = 0.0091). Associations were also found with resting metabolic rate (RMR) (P = 0.042) and plasma leptin levels (P = 0.036). Adjustment for BMI abolished the associations with insulin sensitivity, RMR, and plasma leptin levels. Conclusions: These results confirm that genetic variation at the FTO locus contributes to the etiology of obesity, insulin resistance, and increased plasma leptin levels.
  • 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.