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Start Over Author "PÉRUSSE, LOUIS" Journal obesity research
37 results on '"PÉRUSSE, LOUIS"'

2. The Human Obesity Gene Map: The 2004 Update

Author

Pérusse, Louis, primary, Rankinen, Tuomo, additional, Zuberi, Aamir, additional, Chagnon, Yvon C., additional, Weisnagel, S. John, additional, Argyropoulos, George, additional, Walts, Brandon, additional, Snyder, Eric E., additional, and Bouchard, Claude, additional

Published
2005
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3. The Human Obesity Gene Map: The 2003 Update

Author

Snyder, Eric E., primary, Walts, Brandon, additional, Pérusse, Louis, additional, Chagnon, Yvon C., additional, Weisnagel, S. John, additional, Rankinen, Tuomo, additional, and Bouchard, Claude, additional

Published
2004
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7. Role of Ghrelin Polymorphisms in Obesity Based on Three Different Studies

Author

Ukkola, Olavi, primary, Ravussin, Eric, additional, Jacobson, Peter, additional, Pérusse, Louis, additional, Rankinen, Tuomo, additional, Tschöp, Matthias, additional, Heiman, Mark L., additional, Leon, Arthur S., additional, Rao, D.C., additional, Skinner, James S., additional, Wilmore, Jack H., additional, Sjöström, Lars, additional, and Bouchard, Claude, additional

Published
2002
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13. The Human Obesity Gene Map: The 2000 Update

Author

Pérusse, Louis, primary, Chagnon, Yvon C., additional, Weisnagel, S. John, additional, Rankinen, Tuomo, additional, Snyder, Eric, additional, Sands, John, additional, and Bouchard, Claude, additional

Published
2001
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23. Abdominal Visceral Fat is Associated with aBclI Restriction Fragment Length Polymorphism at the Glucocorticoid Receptor Gene Locus

Author

Buemann, Benjamin, primary, Vohl, Marie-Claude, additional, Chagnon, Monique, additional, Chagnon, Yvon C., additional, Gagnon, Jacques, additional, Pérusse, Louis, additional, Dionne, France, additional, Després, Jean-Pierre, additional, Tremblay, Angelo, additional, Nadeau, André, additional, and Bouchard, Claude, additional

Published
1997
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34. Relation Between BglIIPolymorphism in 3β‐Hydroxysteroid Dehydrogenase Gene and Adipose Tissue Distribution in Humans

Author

Vohl, Marie‐Claude, Dionne, France T., Pérusse, Louis, Dériaz, Olivier, Chagnon, Monique, and Bouchard, Claude

Abstract

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 BglII 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 age2within 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 BglII 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.

Published
1994
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35. Abdominal Visceral Fat is Associated with a BclI Restriction Fragment Length Polymorphism at the Glucocorticoid Receptor Gene Locus

Author

Buemann, Benjamin, Vohl, Marie‐Claude, Chagnon, Monique, Chagnon, Yvon C., Gagnon, Jacques, Pérusse, Louis, Dionne, France, Després, Jean‐Pierre, Tremblay, Angelo, Nadeau, André, and Bouchard, Claude

Abstract

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.

Published
1997
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36. The peroxisome proliferator-activated receptor alpha L162V mutation is associated with reduced adiposity.

Author

Bossé Y, Després JP, Bouchard C, Pérusse L, and Vohl MC

Subjects
Abdomen, Adult, Alleles, Body Constitution, Body Mass Index, Body Weight, DNA analysis, Female, Genotype, Humans, Male, Middle Aged, Polymerase Chain Reaction, Tomography, X-Ray Computed, Adipose Tissue, Body Composition genetics, Mutation, Receptors, Cytoplasmic and Nuclear genetics, Transcription Factors genetics
Abstract

Objective: To determine the contribution of the peroxisome proliferator-activated receptor alpha (PPARalpha) 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 PPARalpha 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/m(2)): 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 (cm(2)): 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/m(2) 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 PPARalpha V162 allele is associated with reduced adiposity and has a substantial population-attributable risk.

Published
2003
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37. Effects of beta2-adrenergic receptor gene variants on adiposity: the HERITAGE Family Study.

Author

Garenc C, Pérusse L, Chagnon YC, Rankinen T, Gagnon J, Borecki IB, Leon AS, Skinner JS, Wilmore JH, Rao DC, and Bouchard C

Subjects
Adipose Tissue, Body Mass Index, Female, Genotype, Humans, Linkage Disequilibrium, Male, Physical Endurance physiology, Polymorphism, Genetic, Skinfold Thickness, Tomography, X-Ray Computed, Black People genetics, Body Composition genetics, Obesity genetics, Receptors, Adrenergic, beta genetics, White People genetics
Abstract

We investigated whether the Arg16Gly and Gln27Glu polymorphisms of the beta2-adrenergic receptor gene were associated with body-fat and fat-distribution phenotypes measured before and in response to a 20-week endurance-training program. BMI, fat mass (FAT), percentage of body fat (%FAT), sum of eight skinfolds (SF8), and abdominal fat areas assessed by computed tomography were measured in adult sedentary white and black participants of the HERITAGE Family Study. Evidence of gene-by-obesity interaction was found in whites for several adiposity phenotypes measured before training. Analyses performed separately in nonobese and obese subjects revealed that obese men carrying the Glu27 allele have lower fat accumulation (BMI, FAT, and %FAT) than noncarriers. Among white obese women, Gly16Gly homozygotes had a lower fat accumulation (BMI, FAT, and SF8) than Arg16Gly and Arg16Arg carriers. In response to endurance training, white women with the Arg16Arg genotype exhibited a greater reduction in BMI, FAT, and %FAT. Results observed in blacks were mostly negative. These results suggest that polymorphisms in the beta2-adrenergic receptor gene influence the amount of body fat in white obese men (Gln27Glu) and women (Arg16Gly), as well as the changes in adiposity in response to endurance training in white women (Arg16Gly).

Published
2003
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