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Personne :
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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  • PublicationAccès libre
    The challenge of stratifying obesity : attempts in the Quebec family study
    (Frontiers Research Foundation, 2019-10-10) Guénard, Frédéric; Bouchard, Claude; Toro Martin, Juan de; Pérusse, Louis; Tremblay, Angelo; Vohl, Marie-Claude
    Background and aims: Obesity is a major health problem worldwide. Given the heterogeneous obesity phenotype, an optimal obesity stratification would improve clinical management. Since obesity has a strong genetic component, we aimed to develop a polygenic risk score (PRS) to stratify obesity according to the genetic background of the individuals. Methods: A total of 231 single nucleotide polymorphisms (SNP) significantly associated to body mass index (BMI) from 21 genome-wide association studies were genotyped or imputed in 881 subjects from the Quebec Family Study (QFS). The population was randomly split into discovery (80%; n = 704) and validation (20%; n = 177) samples with similar obesity (BMI ≥ 30) prevalence (27.8% and 28.2%, respectively). Family-based associations with obesity were tested for every SNP in the discovery sample and a weighed and continuous PRS231 was constructed. Generalized linear mixed effects models were used to test the association of PRS231 with obesity in the QFS discovery sample and validated in the QFS replication sample. Furthermore, the Fatty Acid Sensor (FAS) Study (n = 141; 27.7% obesity prevalence) was used as an independent sample to replicate the results. Results: The linear trend test demonstrated a significant association of PRS231 with obesity in the QFS discovery sample (ORtrend = 1.19 [95% CI, 1.14-1.24]; P = 2.0x10-16). We also found that the obesity prevalence was significantly greater in the higher PRS231 quintiles compared to the lowest quintile. Significant and consistent results were obtained in the QFS validation sample for both the linear trend test (ORtrend = 1.16 [95% CI, 1.07-1.26]; P = 6.7x10-4), and obesity prevalence across quintiles. These results were partially replicated in the FAS sample (ORtrend = 1.12 [95% CI, 1.02-1.24]; P = 2.2x10-2). PRS231 explained 7.5%, 3.2%, and 1.2% of BMI variance in QFS discovery, QFS validation, and FAS samples, respectively. Conclusions: These results revealed that genetic background in the form of a 231 BMI-associated PRS has a significant impact on obesity, but a limited potential to accurately stratify it. Further studies are encouraged on larger populations.
  • 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
    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
    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.
  • PublicationRestreint
    Association between olfactory receptor genes, eating behavior traits and adiposity : results from the Quebec Family Study
    (Pergamon Press, 2011-10-25) Drapeau, Vicky; Choquette, Anne.; Bouchard, Claude; Pérusse, Louis; Tremblay, Angelo; Lemieux, Simone; Vohl, Marie-Claude; Bouchard, Luigi
    Obesity is a major health problem that can be influenced by eating behaviors. Evidence suggests that the sensory properties of food influence eating behaviors and lead to overeating and overweight. A previous genome-wide linkage scan for eating behavior traits assessed with the Three-Factor Eating Questionnaire (cognitive dietary restraint, disinhibition and hunger) performed in the Quebec Family Study (QFS) revealed a quantitative trait locus for disinhibition on chromosome 19p13. This region encodes a cluster of seven olfactory receptor (OR) genes, including OR7D4, previously associated with odor perceptions. Direct sequencing of the OR7D4 gene revealed 16 sequence variants. Nine OR7D4 sequence variants with minor allele frequency (MAF) > 1% as well as 100 SNPs spanning the cluster of OR genes on 19p13 were tested for association with age- and sex-adjusted eating behaviors as well as adiposity traits in 890 subjects. One OR7D4 sequence variant (rs2878329 G > A) showed evidence of association with reduced levels of adiposity (p = 0.03), cognitive dietary restraint (p = 0.05) and susceptibility to hunger (p = 0.008). None of the OR7D4 SNPs was associated with disinhibition, but a SNP (rs2240927) in another OR gene (OR7E24) showed evidence of association (p = 0.03). Another SNP in the OR7G3 gene (rs10414255) was also found to be associated with adiposity and eating behaviors. These results are the first to suggest that variations in human olfactory receptor genes can influence eating behaviors and adiposity. The associations reported in the present study should be interpreted with caution considering the number of tests performed and considered as potential new hypotheses about the effects OR polymorphisms on eating behaviors and obesity that need to be further explored in other populations.
  • PublicationRestreint
    Relation between a BglII polymorphism in 3 beta-hydroxysteroid dehydrogenase gene and adipose tissue distribution in humans
    (North American Association for the Study of Obesity, 1994-09-01) Bouchard, Claude; Dionne, France T.; Pérusse, Louis; Dériaz, Olivier; Vohl, Marie-Claude; Chagnon, Monique
    The aim of this study was to investigate the association between a restriction fragment length polymorphism (RFLP) at the 3β‐hydroxysteroid dehydrogenase locus and adipose tissue distribution pheno‐types. A total of 132 unrelated individuals from the Quebec Family Study were followed prospectively for an average period of 11.3 years. The Bgl II polymorphism in exon 4 of the 3β‐HSD gene was detected by PCR. Body mass, body fat, and regional fat distribution indicators were adjusted for age and age2 within each gender. Associations were assessed in unrelated adults with ANOVA across three genotypes. No association was found for the indicators of body mass, body fat, and regional distribution of adipose tissue measured in 1992. In women, the changes (difference between data collected in 1992 and at entry) in the sum of six skinfolds (p=0.04), abdominal skinfold (p=0.01), and abdominal skinfold adjusted (p=0.03) for the sum of six skinfolds at entry were related to the Bgl II polymorphism at the 3β‐HSD locus. These relations were not found in men, but they gained less body mass and body fat over the 11.3‐year period. This suggests that sequence variation at the 3β‐HSD locus or in neighboring genes on chromosome 1 may contribute to individual differences in body fat content and adipose tissue distribution in adult women, particularly in abdominal adipose tissue deposition as they grow older and gain body fat.