Obesity may have nothing to do at all with eating a lot. A new study done by researchers from the Massachusetts Institute of Technology and the Beth Israel Deaconess Medical Center solved a puzzle about FTO, the gene region associated with obesity. For years, scientists have been trying to understand how the obesity gene controlled appetite, but no direct association has been established.
"Many studies attempted to link the FTO region with brain circuits that control appetite or propensity to exercise," Melina Claussnitzer, lead study author and instructor at Beth Israel Deaconess Medical Centerl, said in a press release. "Our results indicate that the obesity-associated region acts primarily in adipocyte progenitor cells in a brain-independent way."
The researchers discovered that a certain version of FTO turns on the genes IRX3 and IRX5. These genes then turn off thermogenesis, the process wherein fat cells release energy as heat instead of storing it as fat. With thermogenesis turned off, fat accumulates in the body and obesity sets in.
One major discovery in the research is that the signatures of obesity can be reversed in humans. This means that the pathway that leads to obesity can be switched off, opening the door to develop new treatments for those suffering from obesity.
"By manipulating this new pathway, we could switch between energy storage and energy dissipation programs at both the cellular and the organismal level, providing new hope for a cure against obesity," Manolis Kellis, senior study author and MIT professor of computer science, said in the press release.
However, the study findings do not encompass the whole mechanism of obesity, and other genes may be involved. Food and exercise are still factors to consider in maintaining a healthy weight. According to Kellis, a person who has the gene is not automatically destined to become obese but is only predisposed to it, the Associated Press reported.
"For the first time, genetics has revealed a mechanism in obesity that was not really suspected before," Claussnitzer said, adding that the new study challenges a popular idea that people get obese by their own choice "because they choose to eat too much or not exercise."
Evan Rosen, professor of medicine at Harvard Medical School, praised the research team's findings.
"The researchers present a near-complete unveiling of how a genetic risk allele in a noncoding region of the genome really works," Rosen told MIT. "It's really an extraordinary piece of science, and it provides a template for how we should be approaching these genetic variants in all disease areas."
The study was published in the Aug. 19 issue of the New England Journal of Medicine.
