By Vishakha Sonawane, International Business Times, Aug 22, 2015 – Scientists at the Massachusetts Institute of Technology (MIT) and Harvard Medical School have identified how an important gene associated with obesity contributes to weight gain. This genetic pathway controls metabolism by inducing fat cells to control fat or burn it, and if the gene is flawed it makes people fat, the new research found.
Experiments conducted on mice and human cells showed that by adjusting the gene FTO, which was discovered in 2007, researchers could increase the rate of metabolism and balance fat content in the body. The findings could pave way for different methods to tackle obesity, a condition that affects nearly 35 percent of Americans.
“Obesity has traditionally been seen as the result of an imbalance between the amount of food we eat and how much we exercise, but this view ignores the contribution of genetics to each individual’s metabolism,” the study’s senior author Manolis Kellis, a computer science professor at MIT said, in a statement released Wednesday.
According to the Centers for Disease Control and Prevention, statistics show that 17 percent of children in the U.S. are obese. Childhood obesity among preschoolers is more common among those from lower-income families, according to the CDC.
For the study, scientists gathered fat samples from Europeans having both the normal and faulty FTO gene. They found that the DNA code of the FTO gene switched on two other associated genes in obese people, causing these genes to stop burning fat through thermogenesis — a process where excess fat is removed through body heat.
Researchers blocked the flawed gene’s effect in mice and found they became considerably lean despite being on a high-fat diet. These mice burned more energy even when asleep. “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,” Kellis said.
The researchers, who published the study in the New England Journal of Medicine, are also using their findings to understand the connections of other disease-associated regions in the human genome.