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TISSUE-SPECIFIC STEM CELLS

Adipogenic Human Adenovirus Ad-36 Induces Commitment, Differentiation, and Lipid Accumulation in Human Adipose-Derived Stem Cells

^aPennington Biomedical Research Center, Louisiana State University System, Baton Rouge, Louisiana, USA;
^bObesity and Diabetes Clinical Research Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix, Arizona, USA;
^cBaker Heart Research Institute, Melbourne, Australia;
^dWayne State University, Detroit, Michigan, USA

Key Words. Obesity • Adiposity • Adipogenesis • Infectobesity • Lipogenesis • Adipocyte progenitors

Correspondence: Correspondence: Nikhil V. Dhurandhar, Ph.D., Infections and Obesity Laboratory, Pennington Biomedical Research Center, Louisiana State University System, 6400 Perkins Road, Baton Rouge, Louisiana 70808, USA. Telephone: 225-763-2741; Fax: 225-763-3030; e-mail: nikhil.dhurandhar{at}pbrc.edu

Received on October 15, 2007; accepted for publication on January 4, 2008.

First published online in STEM CELLS EXPRESS  January 17, 2008.


Human adenovirus Ad-36 is causatively and correlatively linked with animal and human obesity, respectively. Ad-36 enhances differentiation of rodent preadipocytes, but its effect on adipogenesis in humans is unknown. To indirectly assess the role of Ad-36-induced adipogenesis in human obesity, the effect of the virus on commitment, differentiation, and lipid accumulation was investigated in vitro in primary human adipose-derived stem/stromal cells (hASC). Ad-36 infected hASC in a time- and dose-dependent manner. Even in the presence of osteogenic media, Ad-36-infected hASC showed significantly greater lipid accumulation, suggestive of their commitment to the adipocyte lineage. Even in the absence of adipogenic inducers, Ad-36 significantly increased hASC differentiation, as indicated by a time-dependent expression of genes within the adipogenic cascade—CCAAT/Enhancer binding protein-β, peroxisome proliferator-activated receptor-, and fatty acid-binding protein—and consequentially increased lipid accumulation in a time- and viral dose-dependent manner. Induction of hASC to the adipocyte state by Ad-36 was further supported by increased expression of lipoprotein lipase and the accumulation of its extracellular fraction. hASC from subjects harboring Ad-36 DNA in their adipose tissue due to natural infection had significantly greater ability to differentiate compared with Ad-36 DNA-negative counterparts, which offers a proof of concept. Thus, Ad-36 has the potential to induce adipogenesis in hASC, which may contribute to adiposity induced by the virus.

Disclosure of potential conflicts of interest is found at the end of this article.

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