TY - JOUR
T1 - Genome scan for childhood and adolescent obesity in German families
AU - Saar, Kathrin
AU - Geller, Frank
AU - Rüschendorf, Franz
AU - Reis, André
AU - Friedel, Susann
AU - Schäuble, Nadine
AU - Nürnberg, Peter
AU - Siegfried, Wolfgang
AU - Goldschmidt, Hans Peter
AU - Schäfer, Helmut
AU - Ziegler, Andreas
AU - Remschmidt, Helmut
AU - Hinney, Anke
AU - Hebebrand, Johannes
PY - 2003/2/1
Y1 - 2003/2/1
N2 - Objective. Several genome scans have been performed for adult obesity. Because single formal genetic studies suggest a higher heritability of body weight in adolescence and because genes that influence body weight in adulthood might not be the same as those that are relevant in childhood and adolescence, we performed a whole genome scan. Methods. The genome scan was based on 89 families with 2 or more obese children (sample 1). The mean age of the index patients was 13.63 ± 2.75 years. A total of 369 individuals were initially genotyped for 437 microsatellite markers. A second sample of 76 families was genotyped using microsatellite markers that localize to regions for which maximum likelihood binomial logarithm of the odd (MLB LOD) scores on use of the concordant sibling pair approach exceeded 0.7 in sample 1. Results. The regions with MLB LOD scores >0.7 were on chromosomes 1p32.3-p33, 2q37.1-q37.3, 4q21, 8p22, 9p21.3, 10p11.23, 11q11-q13.1, 14q24-ter, and 19p13-q12 in sample 1; MLB LOD scores on chromosomes 8p and 19q exceeded 1.5. In sample 2, MLB LOD scores of 0.68 and 0.71 were observed for chromosomes 10p11.23 and 11q13, respectively. Conclusion. We consider that several of the peaks identified in other scans also gave a signal in this scan as promising for ongoing pursuits to identify relevant genes. The genetic basis of childhood and adolescent obesity might not differ that much from adult obesity.
AB - Objective. Several genome scans have been performed for adult obesity. Because single formal genetic studies suggest a higher heritability of body weight in adolescence and because genes that influence body weight in adulthood might not be the same as those that are relevant in childhood and adolescence, we performed a whole genome scan. Methods. The genome scan was based on 89 families with 2 or more obese children (sample 1). The mean age of the index patients was 13.63 ± 2.75 years. A total of 369 individuals were initially genotyped for 437 microsatellite markers. A second sample of 76 families was genotyped using microsatellite markers that localize to regions for which maximum likelihood binomial logarithm of the odd (MLB LOD) scores on use of the concordant sibling pair approach exceeded 0.7 in sample 1. Results. The regions with MLB LOD scores >0.7 were on chromosomes 1p32.3-p33, 2q37.1-q37.3, 4q21, 8p22, 9p21.3, 10p11.23, 11q11-q13.1, 14q24-ter, and 19p13-q12 in sample 1; MLB LOD scores on chromosomes 8p and 19q exceeded 1.5. In sample 2, MLB LOD scores of 0.68 and 0.71 were observed for chromosomes 10p11.23 and 11q13, respectively. Conclusion. We consider that several of the peaks identified in other scans also gave a signal in this scan as promising for ongoing pursuits to identify relevant genes. The genetic basis of childhood and adolescent obesity might not differ that much from adult obesity.
UR - http://www.scopus.com/inward/record.url?scp=0037313906&partnerID=8YFLogxK
U2 - 10.1542/peds.111.2.321
DO - 10.1542/peds.111.2.321
M3 - Journal articles
C2 - 12563058
AN - SCOPUS:0037313906
SN - 0031-4005
VL - 111
SP - 321
EP - 327
JO - Pediatrics
JF - Pediatrics
IS - 2
ER -