Published in the Sept. 5 issue of the journal Cell Metabolism by researchers at the University of Texas Southwestern Medical Center, the report looks at the role played by a single gene in fat formation.
Greater activity in the "adipose" gene -- first discovered in fruit flies 50 years ago -- was found to keep fruit flies, worms and mice skinny, regardless of how much they ate.
"It could explain why so many people struggle to lose weight and suggests an entirely new direction for developing medical treatments that address the current epidemic of diabetes and obesity," said Dr. Jonathan Graff, associate professor of developmental biology and internal medicine at UT Southwestern, the senior author of the study.
The gene was manipulated by turning it on and off at different stages of the animal's life and in different parts of the body.
In genetically engineered mice, researchers found that increased activity in the gene led to leaner, healther mice, even if they ate more than regular mice. Mice with reduced gene activity were fatter, less healthy and had diabetes.
There may be a drawback to having the "skinny" gene, however. When flies with the gene were placed in famine-like conditions, they did poorly. The gene is beneficial during times of abundance, when, according to Graff, "too much fat in times of plenty has deleterious consequences."
The most promising result, however, seemed to be that different combinations of the gene's variants led to a range of body types.
"This is good news for potential obesity treatments, because it's like a volume control instead of a light switch; it can be turned up or down, not just on or off," Graff said. "Eventually, of course, the idea is to develop drugs to target this system, but that's in the years to come."
While the gene is known to be present in humans, it is not known if the gene works similarly in people.
But Graff remains hopeful, "Maybe if you could affect this gene, even just a little bit, you might have a beneficial effect on fat."
