The critical region for childhood-obesity onset was located within 80 kilobases of exon 1 of BDNF; serum BDNF concentrations were 50% lower in patients with heterozygous BDNF deletions (P=.001), according to the researchers.
“Hyperleptinemia is a hallmark of almost all forms of obesity; thus, understanding the role of downstream mediators of leptin action such as BDNF holds promise for laying the groundwork for the development of new pharmaceutical approaches to the global obesity epidemic,” the researchers wrote.
“Further studies are needed to assess the potential therapeutic role of BDNF replacement in people in whom insufficient BDNF protein is produced and the potential contributions of more common allelic variants at the locus for susceptibility to obesity among people in the general population.” Read more at endocrinetoday.com
Posted By:
Monday, October 27th 2008 at 7:39PM
You can also
click
here to view all posts by this author...
