Washington, Mar 12 : A research team from the Children's Hospital and the University of Pennsylvania School of Medicine has further refined the marker to a common obesity gene called FTO - something that may help identify its role in obesity in various human populations worldwide
This finding of the study, led by Struan Grant, Ph.D., and Hakon Hakonarson, M.D., Ph.D., both of the Center for Applied Genomics of The Children's Hospital of Philadelphia, suggest that that the gene variant, identified in DNA from African American children, may be a tag of an ancient mutation that started in Africa, where humans originated.
The team of researchers were studying the FTO gene identified by a British group in 2007 as raising the risk of adult and childhood obesity. Family studies have indicated that obesity has a genetic component in addition to environmental influences.
In 2007, the British group had originally found the FTO gene variant among obese Caucasians. In order to replicate the previous finding, the researchers in the current study used a genetic screening technique by using samples from Caucasian and African American children, who were either obese or not.
The sane gene variant was found to be present among Caucasian children, but not among the African American children. On the contrary, a second variant, found in both Caucasians and African Americans, was the only marker significantly linked to obesity among the African American children.
Both these variants were changes to a single chemical base along the DNA strand, which geneticists call single nucleotide polymorphisms, or SNPs.
According to Grant, for genomics researchers, the findings mean that if other investigators look only for the first SNP in subjects with African ancestry, they would find no association with obesity. The second SNP may have deep roots in evolutionary history.
The researchers already have multiple lines of evidence suggesting that humans originated in Africa, and this SNP may be related to an original mutation in the distant past that triggered a human predisposition to obesity.
Grant also said that the fact that mutations in the FTO gene carry a comparable risk of obesity in both children and adults indicates that the gene may be primarily associated with obesity that begins in childhood. He added that future medical treatments may benefit patients by targeting the FTO gene pathway, although such treatments await a better understanding of the underlying biology of obesity.
The findings of this study are reported in the recent issue of the journal Public Library of Science One.