New evidence linking viruses to obesity
Common virus may contribute to obesity in some people
Central Obesity
Last September, I noted that the epidemiology of modern obesity (in the last couple decades) strongly suggests transmissible or pervasive environmental factors–more persavive even than junk food and sedentary behavior–at work in its etiology. Now, Magdalena Pasarica, M.D., Ph.D., of the Pennington Biomedical Research Center and her colleagues are reporting at the American Chemical Society meeting that adenovirus-36 (Ad-36), a common form of this common human-infecting virus, is capable of differentiating adult human stem cells into fat:
In the current study, Pasarica and her associates obtained adult stem cells from fatty tissue from a broad cross-section of patients who had undergone liposuction. Half of the stem cells were exposed to Ad-36 and the other half were not exposed to the virus. After about a week of growth in tissue culture, most of the virus-infected adult stem cells developed into fat cells, whereas the non-infected stem cells did not, the researchers say. Funded by the National Institutes of Health (NIH), Dr. Dhurandhar’s group recently identified a gene in the Ad-36 virus that appears to be involved in causing fat accumulation observed in infected animals. That gene, called E4Orfl, is now emerging as a promising target for future human therapies, such as vaccines and anti-viral medicines, aimed at preventing or inhibiting the obesity virus, she says.
About 30% of obese people are infected with Ad-36, compared with 11% of nonobese people. While this evidence doesn’t prove an etiologic link between Ad-36 and obesity–that ultimately requires evidence that eradication of the virus or its effectors ameliorates obesity–it is a necessary step up the proof ladder. Personally, I’m thinking that environmental factors that alter the gut microbiome (antibiotics? environmental pollutants?), increasing the efficiency of intestinal energy absorption, are more likely culprits than adenovirus, but then again, multiple etiologic agents are likely contributing.
