Of considerable interest is the role of the genes in the predisposition to become obese. Among the lines of evidence for a role of the genes, one must include the human linkage studies. Two genomic scans have been reported to date, one from the Pima Indian sibling study and the second from the San Antonio Family Heart Study. In the former, the strongest evidence for linkage with body fat was with markers on chromosome 11q21-q22, 6p21.3 and 3p24.2-p22, while in the latter it was with markers on 2p21. Evidence for linkage with markers on 7q33 was obtained in all family studies with the only apparent exception being the Pima Indians.
Our own results from the Quebec family Study suggests that there are linkages between body fat, as assessed from hydrodensitometry, and markers on 1p32-p22. In addition, significant linkages have also been obtained in QFS for markers spanning the region from the ADA locus to the MC3R locus on 20q12-q13 and with MC5R on 18p11.2. Other linkages have been reported in the past but they are generally based on weaker evidence.
All these results will be summarized and discussed with respect to candidate genes and genome wide scan initiatives. The stage is now set for major advances to occur in the understanding of the genetic and molecular basis of the responsiveness to various dietary regimens and of complex diseases such as human obesity.
Note to reporters: This is one of four fact sheets about the symposium presentation.
News release also available. Contact: 214-706-1340.