Obesity Goes Viral?



Nikhil Dhurandar

Nikhil Dhurandar, PhD

Yes, the rapid spread of obesity around the world is reminiscent of the spread of an infectious diseases (albeit in slow motion), but is an obesity infection even possible?

Well, yesterday’s obesity news in the media was once again all about the obesity virus. These media reports were prompted by a new paper by Miloni Rathod and colleagues from Wayne State University, Detroit and the Pennington Biomedical Research Centre, Baton Rouge, published in Obesity.

This report is a follow-up to the many excellent studies from Nikhil Dhurandar’s group, which first suggested that the rather common human Ad36 virus may play a role in adipogenesis (formation of fat cells).

In the present study, using cultured mouse preadipocytes, the researchers demonstrated the following:

1) That the adenovirus Ad36 but not Ad2 stimulates fat accumulation as well as the expression of specific early, intermediate and late adipogenic marker genes in cultured mouse preadipocytes.

2) That treatment of adenovirus Ad36-infected cells with an antiadenoviral agent reduces fat accumulation in preadipocytes, demonstrating that viral mRNA expression is required for the process.

3) That although infection with adenovirus Ad36 amplifies the adipogenic response to a differentiation cocktail (containing insulin and other promoters of adipogenesis), this cocktail is not essential for Ad36 to induce formation of fat cells.

Thus, clearly, this human adenovirus can infect mouse cells to promote fat cell formation and it certainly appears worth the effort to try to elucidate exactly how this virus has this effect.

But what does this mean for human obesity?

Firstly, the Ad36 virus is extremely common and many people probably carry it – whether or not carrying this virus actually means that you are likely to gain more weight remains to be seen.

Secondly, it is important to remember that formation of fat cells in itself may not be a bad thing. After all, fat cells are the safest place to store extra calories. It is indeed widely believed that failure to accomodate excess calories in fat tissue (as a result of limited fat-cell formation) may promote fat deposition in other tissues (liver, muscle, heart), thereby promoting the development of metabolic risk factors like insulin resistance. Thus, infection with Ad36 may cause you to grow more fat cells, but may very well also turn out to actually decrease your risk for diabetes and other metabolic problems.

Thus, it will certainly be a while before antiviral treatments or even vaccinations will make it into our clinical armamentum for obesity prevention or management.

Nevertheless, it certainly is a good story and illustrates the fact that the study of obesity (and its origin) is anything but as simple or straightforward as many people believe.

AMS
Edmonton, Alberta