Personne : Pérusse, Louis
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Université Laval. Département de kinésiologie
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- PublicationRestreintPlasminogen-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, LuigiObjective: 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.
- PublicationRestreintInfluences 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-PierreBackground: 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.
- PublicationRestreintA 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, JohnInflammation 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.
- PublicationAccès libreThe 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, PatrickThe 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.
- PublicationRestreintAssociation 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-ClaudeIt 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.
- PublicationRestreintEvidence 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-ClaudeBackground: 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.
- PublicationRestreintThe peroxisome proliferator-activated receptor α L162V mutation is associated with reduced adiposity(North American Association for the Study of Obesity, 2012-09-06) Bouchard, Claude; Pérusse, Louis; Bossé, Yohan; Vohl, Marie-Claude; Després, Jean-PierreObjective: To determine the contribution of the peroxisome proliferator-activated receptor α (PPARα) L162V mutation to the variation of several indexes of body fatness obtained from healthy adults who participated in the Quebec Family Study. Research Methods and Procedures: The PPARα L162V mutation was determined by a mismatch polymerase chain reaction method. Adiposity phenotypes were obtained by standardized anthropometric measurements, underwater weighing technique, and computed tomography. Results: For all adiposity phenotypes, subjects carrying the V162 allele had lower values compared with L162 homozygotes (HMZs) [BMI (kg/m2): 27.8 ± 7.6 vs. 26.0 ± 5.6, p < 0.05; percentage body fat: 28.5 ± 10.7 vs. 25.7 ± 10.1, p < 0.05; waist circumference (cm): 89.0 ± 18.1 vs. 85.7 ± 15.8, p = 0.07; total computed tomography abdominal fat areas (cm2): 406 ± 221 vs. 359 ± 192, p = 0.15; means ± SD for L162 HMZs vs. V162 carriers, respectively]. Differences in cross-sectional abdominal adipose tissue areas and waist circumference were abolished after adjustment for total body fat mass. Similar trends were observed when results were analyzed by gender, although associations seemed stronger in women. The odds ratio of having a BMI above 30 kg/m2 reached 1.77 (1.02; 3.07, 95% confidence intervals) for L162 HMZs. This risk could be considered marginal on an individual basis, but because 85% of the subjects are affected by this small risk, the impact on the population is important. Discussion: The PPARα V162 allele is associated with reduced adiposity and has a substantial population-attributable risk.
- PublicationRestreintRelation 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, MoniqueThe 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.
- PublicationRestreintEvidence for interaction between PPARG Pro12Ala and PPARGC1A Gly482Ser polymorphisms in determining type 2 diabetes intermediate phenotypes in overweight subjects(Thieme, 2009-06-17) Ruchat, Stéphanie-May; Bouchard, Claude; Pérusse, Louis; Rankinen, Tuomo; Weisnagel, John; Vohl, Marie-ClaudeBackground: The peroxisome proliferator-activated receptor-γ (PPARG) Pro12Ala and the PPARG co-activator-1α (PPARGC1A) Gly482Ser polymorphisms (SNPs) have been associated with type 2 diabetes mellitus (T2DM) risk. We hypothesized that independent and interactive effects of the PPARG Pro12Ala and PPARGC1A Gly482Ser polymorphisms influence T2DM intermediate phenotypes. Material and Methods: PPARG Pro12Ala and PPARGC1A Gly482Ser SNPs were studied in 680 non diabetic subjects who underwent a 75 g oral glucose tolerant test (OGTT). Glucose and insulin plasma levels in the fasting state and derived from the OGTT were included in the present study. Results: We found significant independent effects of the PPARG and PPARGC1A variants on fasting insulin levels (p=0.02 for both), HOMA-IR (p=0.03 and p=0.02, respectively), insulin area under the curve (AUC) (p=0.007 and p=0.006, respectively) and 2-h glucose levels (p=0.02 for PPARGC1A). Furthermore, significant gene-gene interactions were found for fasting insulin, HOMA-IR and insulin AUC (p=0.03 for all). Carriers of the PPARGC1A Gly allele who were also PPARG Ala-carriers had higher fasting insulin levels (p=0.02), HOMA-IR (p=0.01) and insulin AUC (p=0.01) compared to the Ser/Ser-Ala+genotype combination, whereas no differences between the PPARGC1A genotypes among the PPARG Pro/Pro carriers were observed. Conclusion: Together, these results showed that PPARG Pro12Ala and PPARGC1A Gly482Ser variants are associated, alone and in interaction, with insulin and glucose homeostasis and suggest that gene-gene interactions should be taken into account in candidate gene studies of T2DM to identify subjects with markedly different risks of developing the disease.
- PublicationAccès libreLIPE C-60G influences the effects of physical activity on body fat and plasma lipid concentrations : the Quebec Family Study(BioMed Central, 2009-01-01) Garenc, Christophe; Pérusse, Louis; Vohl, Marie-Claude; Bouchard, ClaudeA large body of evidence suggests that the environment plays an important role in the development of obesity. The hormone-sensitive lipase (encoded by the LIPE gene) is an intracellular enzyme that mobilises fat stores in a hormone-stimulated manner. The aim of the present study was to determine the effects of the LIPE C-60G polymorphism on body fat and plasma lipid and lipoprotein concentrations, and to test for its interaction with physical activity. The LIPE C-60G polymorphism was genotyped in 862 subjects from the Quebec Family Study. Body mass index (BMI), fat mass, percentage body fat, abdominal fat areas assessed by computed tomography, and detailed fasting plasma lipid and lipoprotein profiles were measured. Levels of physical activity were estimated using a three-day diary, and a moderate to strenuous physical activity score was retained for this study. The main effects of the LIPE C-60G polymorphism, physical activity and their interaction were determined by regression analyses separately in men and women using the MIXED model procedure. In men, we observed significant gene-physical activity interactions for BMI (p = 0.006), fat mass (p = 0.04), abdominal visceral fat area (p = 0.005) and plasma cholesterol (C) high-density lipoprotein cholesterol (HDL-C) ratio (p = 0.003). A high level of physical activity was associated with reduced adiposity and a lower plasma-C/HDL-C ratio, but only in non-carriers of the genetic variant (G-60 allele). In women, no evidence of a gene by physical activity interaction was observed, except for subcutaneous abdominal fat (p = 0.05). These results suggest that the associations between physical activity and body fat and plasma lipoprotein/lipid concentrations in men are dependent on the LIPE C-60G polymorphism, and highlight the importance of taking into account the role of gene-physical activity interactions in candidate gene studies of obesity and obesity-related traits.