TY - JOUR
T1 - Genome-wide search for genes related to the fat-free body mass in the quebec family study
AU - Chagnon, Yvon C.
AU - Borecki, Ingrid B.
AU - Pérusse, Louis
AU - Roy, Sonia
AU - Lacaille, Michel
AU - Chagnon, Monique
AU - Ho-Kim, My Anh
AU - Rice, Treva
AU - Province, Michael A.
AU - Rao, D. C.
AU - Bouchard, Claude
N1 - Funding Information:
The authors wish to acknowledge the contribution of Guy Fournier and Lucie Allard to the data collection in the QFS, Franqois Michaud and Claude Leblanc for management of the database, and Anne-Marie Bricault for cell culture and preparation of the DNA. The results of this study were obtained, in part, using the program S.A.G.E., which is supported by a US Public Health Service Resource Grant (1P41 RR03655) from the National Center for Research Resources.
Funding Information:
From the Physical Activity Sciences Laboratory, Division of Kinesiology, Department of Social and Preventive Medicine, Faculty of Medicine, Laval University, Ste-Foy, Quebec, Canada; Division of Biostatistics, Washington University School of Medicine, St Louis, MO; and Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA. Submitted March 17, 1999; accepted July 8, 1999. Supported by the Medical Research Council of Canada (PG-11811, MT-13960, and GR-15187), and in part by the Donald B. Brown Research Chair on Obesity funded by the Medical Research Council of Canada and Roche Canada (C.B.). Address reprint requests to Yvon C. Chagnon, PhD, Physical Activity Sciences Laboratory, Kinesiology, PEPS 0212, Department of Social and Preventive Medicine, Laval University, Ste-Foy, Quebec, GIK 7P4 Canada. Copyright © 2000 by W.B. Sounders Company 0026-0495/00/4902-0001510.00/0
PY - 2000
Y1 - 2000
N2 - Fat-free mass (FFM) consists mostly of skeletal muscle and bone tissues, and identification of the genes and molecular mechanisms involved in the control of FFM would have implications for the understanding of sarcopenia and potentially osteoporesis associated with aging, as well as the response to starvation, refeeding, anorexia, and any other conditions in which lean body mass is important. A genome-wide search for genes related to body leanness has been completed in the Quebec Family Study (QFS). Microsatellite markers (N = 292) from the 22 autosomal chromosomes were typed. The mean spacing of the markers was 11.9 centimorgans (cM) (range, <0.1 to 41). FFM was calculated from percent body fat, derived from underwater weighing, and body weight and was adjusted by regression for age and sex effects before analysis. A maximum of 336 sib pairs or 609 pairs of extended relatives were analyzed using single-point Haseman-Elston regression (SIBPAL and RELPAL) and multipoint variance component (SEGPATH) linkage analyses. Significant linkages Were observed on chromosomes 15q25-q26 for a CA repeat within the insulin-like growth factor 1 receptor (IGF1R) gene (Lod Score = 3.56) and at 18q12 with D18S877 (Lod score = 3.53) and D18S535 (Lod score = 3.58), 2 markers located 10 cM apart. A moderately significant linkage was also observed on chromosome 7p15.3 with the marker D7S1808 (Lod score = 2.72). The most obvious candidate genes within the regions identified by these linkages include the IGFIR on 15q and neuropeptide Y (NPY) and growth hormone- releasing hormone (GHRH) receptor on 7p. On 18q, the melanocortin receptor 4 (MC4R) is not likely the candidate gene for the observed linkage. This study represents the first genome-wide search for genes that may be involved in the regulation of the lean component of body mass in humans. (C) 2000 by W.B. Saunders Company.
AB - Fat-free mass (FFM) consists mostly of skeletal muscle and bone tissues, and identification of the genes and molecular mechanisms involved in the control of FFM would have implications for the understanding of sarcopenia and potentially osteoporesis associated with aging, as well as the response to starvation, refeeding, anorexia, and any other conditions in which lean body mass is important. A genome-wide search for genes related to body leanness has been completed in the Quebec Family Study (QFS). Microsatellite markers (N = 292) from the 22 autosomal chromosomes were typed. The mean spacing of the markers was 11.9 centimorgans (cM) (range, <0.1 to 41). FFM was calculated from percent body fat, derived from underwater weighing, and body weight and was adjusted by regression for age and sex effects before analysis. A maximum of 336 sib pairs or 609 pairs of extended relatives were analyzed using single-point Haseman-Elston regression (SIBPAL and RELPAL) and multipoint variance component (SEGPATH) linkage analyses. Significant linkages Were observed on chromosomes 15q25-q26 for a CA repeat within the insulin-like growth factor 1 receptor (IGF1R) gene (Lod Score = 3.56) and at 18q12 with D18S877 (Lod score = 3.53) and D18S535 (Lod score = 3.58), 2 markers located 10 cM apart. A moderately significant linkage was also observed on chromosome 7p15.3 with the marker D7S1808 (Lod score = 2.72). The most obvious candidate genes within the regions identified by these linkages include the IGFIR on 15q and neuropeptide Y (NPY) and growth hormone- releasing hormone (GHRH) receptor on 7p. On 18q, the melanocortin receptor 4 (MC4R) is not likely the candidate gene for the observed linkage. This study represents the first genome-wide search for genes that may be involved in the regulation of the lean component of body mass in humans. (C) 2000 by W.B. Saunders Company.
UR - http://www.scopus.com/inward/record.url?scp=0033976374&partnerID=8YFLogxK
U2 - 10.1016/S0026-0495(00)91299-X
DO - 10.1016/S0026-0495(00)91299-X
M3 - Article
C2 - 10690945
AN - SCOPUS:0033976374
SN - 0026-0495
VL - 49
SP - 203
EP - 207
JO - Metabolism: clinical and experimental
JF - Metabolism: clinical and experimental
IS - 2
ER -