GENOME-WIDE SEARCH FOR GENES RELATED TO ADIPOSITY AND ITS CHANGES WITH ENDURANCE TRAINING IN THE HERITAGE FAMILY STUDY.

1906 A large scale genome-wide search is underway in the HERITAGE Family Study. Microsatellite markers (N=234) from the 22 autosomal chromosomes will be used. Mean spacing of the markers are 19 cM (range 2-29). A preliminary analysis was undertaken on 90 of these markers among which none were located on chromosomes 20 and 21. Phenotypes studied at baseline and in response to a 20 week training program were body mass index, sum of eight skinfold thicknesses, fat mass and percent fat mass (underwater weighing), and plasma leptin levels. All phenotypes were adjusted within race for age and sex, and for baseline values for the training changes. Leptin was also analyzed with or without adjustment for body fat. A maximum of 119 and 358 sib-pairs from Black and Caucasian families, respectively, were studied using a single-point linkage analysis (SIBPAL). On chromosomes 1 and 3, evidence for linkage is observed at baseline and for adiposity changes both in Blacks and Caucasians, whereas for chromosomes 4 and 19, they are observed only in Caucasians with a marker close to the carboxypeptidase E (CPE) gene, and within the low density lipid receptor (LDLR) gene, respectively. Chromosome 16 is linked only to changes in adiposity, in both races, for a marker within RAD (Ras associated to diabetes) gene. We conclude that different genetic loci could contribute to adiposity in sedentary state or in response to training or to both, with race differences. Supported by NIH.