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September 11, 2007
Data from two Centers for Disease Control Surveys, shows that among adults 20-74 the prevalence of obesity increased from 15% in the 1976-1980 survey to 32.9% in the 2003-2004 survey. As many Americans know from their yearly trip to the doctor, obesity is a concern for healthcare providers because it increases a patient's risk for a number of diseases, including heart disease, hypertension, and certain types of cancers.
In fact a 1999 study showed that estimated number of annual deaths attributable to obesity among US adults is approximately 280,000. Now new research, suggests that our weight can be controlled by a single gene, adipose.
“From worms to mammals, this gene controls fat formation,” said Jonathan Graff, of University of Texas Southwestern Medical Center, and lead author on the paper. “It could explain why so many people struggle to lose weight and suggests and entirely new direction for developing medical treatments that address the current epidemic of diabetes and obesity.”
The gene was first discovered 50 years ago in a group of plump fruit flies from Nigeria, by Winifred Doane. The mutant flies were found in a climate marked by cycles of famine. Doane suggested that being highly efficient at fat storage in this environment may have been important for their survival.
Researchers studied how adipose works by looking at the gene in fruit flies, tiny worms, cell cultures, and genetically engineered mice.
In mice the researchers found that increasing adipose activity improved the animals health. They ate as much as normal mice but they were leaner, had diabetes-resistant fat cells, and were better able to control insulin and blood-sugar metabolism. Animals with less adipose activity were fatter, less healthy and had diabetes.
This early stage research may one day give hope for controlling obesity and its associated illnesses.
Resource
David B. Allison; Kevin R. Fontaine; JoAnn E. Manson; June Stevens; Theodore B. VanItallie Annual Deaths Attributable to Obesity in the United States
JAMA, Oct 1999; 282: 1530 - 1538.
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