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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

2 Comments

  1. This whole idea of viruses makes me think seriously about the effect of genetically modified (transgenic crops) foods on obesity and human health. Namely much of the north american corn, soybean and canola crops is transgenic and these plants have small insertions from bacteria and/or viruses as part of the new DNA of the plant (in order to be round-up (glyphosate) ready or to produce bacillus thuringiensis (BT), etc ). What I wonder about is how do our innate intestinal bacteria respond to this novel “food”, and how do these foreign DNA snippets influence our own fat cells, our metabolism or immunity. I have read that some researchers think that obesity has an auto-immune component and I wonder if it is possible that this could be related to these new DNA combinations we are unwittingly ingesting. I was fascinated by Jeffrey Gordon’s work which showed that innoculating the gut flora into sterile mice resulted in obesity if the flora came from obese donors, and normal weight when it came from normal weight donor mice.

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  2. Hi Arya,

    Another great post – I particularly like the discussion of the potential health benefit of adipocyte hyperplasia. I remember being very fascinated with the notion of hypertrophic vs. hyperplastic when I read a couple of paper s from the 1980’s. Very often the thinking is that “fat is bad” – a very myopic viewpoint.

    As a perfect example, look at individuals with complete congenital lipodystrophy (lack of fat tissue) – look very lean and athletic, but due to no fat tissue have astronomically high rates of diabetes, cardiovascular disease, etc. Similar thinking is thought to apply to the metabolically-obese, normal weight individuals – have a predominance of hypertrophied and dysfunctional fat cells, despite not having a high BMI – and have all the health problems commonly thought to be exclusive to those with BMIs > 30 kg/m2. On the other hand, the metabolically normal obese phenotype, is exemplified by numerous small and functional adipocytes, and thus a normal metabolic profile, despite a high BMI.

    Clearly fat is not bad – on the contrary – not having enough functional fat is bad.
    Once again, I will likely post further on this, Arya . This is a tremendously interesting area of literature, and I can’t believe I haven’t even mentioned it on our blog. Thanks for the reminder:)

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