WEDNESDAY, March 12, 2014 (HealthDay News) -- Scientists who identified a gene that appears to be strongly linked with obesity say their discovery could help efforts to find drug treatments for obesity and diabetes.
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"Our data strongly suggest that [the gene] IRX3 controls body mass and regulates body composition," study senior author Marcelo Nobrega, an associate professor of human genetics at the University of Chicago, said in a university news release.
Although the research showed an association between the gene and obesity, it did not prove a cause-and-effect link.
The IRX3 gene was first pinpointed through an analysis of about 150 brain samples from people of European ancestry, according to the study, which was published online March 12 in the journal Nature.
To verify the role of IRX3 in obesity, the researchers created mice without the gene and found that they weighed about 30 percent less than normal mice. Much of this weight difference was due to reduced amounts of fat in the mice without the IRX3 gene.
"These mice are thin. They lose weight primarily through the loss of fat, but they are not runts," study co-author Chin-Chung Hui, a professor of molecular genetics at the University of Toronto, said in the news release.
The researchers also found that mice with altered function of the IRX3 gene in the hypothalamus -- the part of the brain that controls eating and energy output -- were as lean as mice that lacked the gene.
This suggests that the gene's activity in the hypothalamus controls body mass and composition in mice, and that genetic predisposition to obesity is wired in the brain, according to the study authors.
Findings from animal studies often can't be replicated in human trials, however.
Previous research has suggested that mutations in a gene called FTO play a strong role in determining obesity risk in people. But this study found that the obesity-related mutations in FTO interact with IRX3, and that FTO itself has only a minor effect on obesity risk.
-- Robert Preidt
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SOURCE: University of Chicago, news release, March 12, 2014
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