Scientists at the 234th national meeting of the American Chemical Society in Boston, Massachusetts this week presented the results of a study that suggests a common virus could be partly responsible for the obesity epidemic that is sweeping across America and other nations. They hope their findings will develop antiviral medication to treat “viral obesity”.
According to the National Institutes of Health (NIH), some 97 million adult Americans are obese. Obesity increases risk of many illnesses, including type 2 diabetes, heart disease, stroke, and osteoarthritis.
So far scientists have shown that genetic predisposition increases risk of obesity, as do other contributory factors including over-eating, eating foods high in fat, lack of physical exercise, genetics, and some medications.
In this latest study, researchers used lab experiments to show that infection with a common virus that causes respiratory and eye infections in humans, called human adenovirus-36 (Ad-36) turns adult stem cells retrieved from fat tissue into fat cells. But stem cells that were not exposed to Ad-36 did not turn into fat cells.
The scientists have also discovered that a specific gene in the virus causes the transformation from stem cells into fat cells.
Presenting the results of the study was Dr Magdalena Pasarica, obesity researcher at the Pennington Biomedical Research Center, part of Louisiana State University:
“We’re not saying that a virus is the only cause of obesity, but this study provides stronger evidence that some obesity cases may involve viral infections.”
Pasarica explained that:
“Not all infected people will develop obesity. We would ultimately like to identify the underlying factors that predispose some obese people to develop this virus and eventually find a way to treat it.”
Pasarica and colleagues took adult stem cells from the fatty tissue of a range of patients who had undergone liposuction. They exposed half of the stem cells to Ad-36, but not the other half.
After a week, most of the virus infected stem cells had transformed into fat cells, but the ones that were not infected had not changed.
Pasarica was involved in an earlier study led by Dr Nikhil Dhurandhar, now associate professor at Pennington Biomedical Research Center. The study showed that Ad-36 caused fat accumulation in animals infected with the virus. The research team then carried out an epidemiological study that showed 30 per cent of obese people were infected with Ad-36, compared with only 11 per cent of lean people.
It was not until this latest study that they were able to show how the virus actually increases fat in humans, according to the researchers.
The research team has also identified a gene in the Ad-36 virus, called E4Orfl, that seems to play a key role in switching on the fat accumulation process in infected animals. The gene could be a target for a range of human therapies, including vaccines and anti-virals, to treat obesity, said Pasarica.
Apart from discovering that stem cells turn into fat cells in the presence of this gene, the scientists know little else about the virus, and they don’t rule out the possibility that other viruses could have similar effects, creating a picture of obesity as being a complex disease involving different viruses.
For instance, they don’t know how long the fat converting effects remain in the body once the virus has left it. There is a slight clue in a recent animal study where infected animals remained obese up to 6 months after the virus had cleared.
Pasarica said a lot more studies were needed, especially in humans. The team is carrying out further investigations into the factors that trigger obesity in some people with the virus while other infected people don’t become obese.
Written by: Catharine Paddock