Image courtesy of Boston Children's Hospital
Scientists have discovered a gene mutation that causes severe obesity in mice. Here, sister mice with normal (right) or mutant (left) Mrap2 gene.
Medically, obesity is now considered a disease. Socially, the condition is regarded differently. In the latter realm, being extremely overweight can seem like a symptom of laziness or lack of willpower.
Research into the genetics of obesity, however, is revealing that judgment may be unfair. Researchers at Boston Children’s Hospital have discovered a gene that, when deleted, causes extreme obesity in mice. Although an initial survey showed that disease-causing mutations in the gene are quite rare in people, scientists think that less severe mutations in this and other rare genes associated with obesity may cause subtle differences in energy regulation and metabolism. Those differences may cause some people to be predisposed to weight gain.
In an unusual twist, the mice in the study published Thursday in the journal Science didn’t gain weight simply because they ate more. Rodents lacking the gene must be fed about 15 percent less than normal mice to have the same amount of weight gain.
“The mice we have made that are obese, while they’re children and adolescents and in that phase, they’re getting very obese, but not eating more than brothers and sisters,” said Dr. Joseph Majzoub, chief of endocrinology at Children’s Hospital. “It’s quite different from other types of obesity.”
Dr. Michael Schwartz, director of the Diabetes and Obesity Center of Excellence at the University of Washington, said that the new study was a valuable addition to the growing knowledge about the genetic underpinnings of obesity. Schwartz, who was not involved in the work, said that in addition to genes that cause severe obesity, there are genes that protect against gaining weight. The genetic predisposition to gain weight was probably influenced not only by genes that make people gain weight, he said, but in flaws in those that protect against gaining weight.