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Endothelial progenitor cells in overweight: exhausted long before the summit?

International Journal of Obesity volume 33, page 702 (2009)Cite this article

With great interest, we read the article by MacEneaney et al.1 that was published very recently in this journal. The authors showed in a well-designed study the influence of overweight and obesity on endothelial progenitor cells (EPCs) in adults. EPCs are bone marrow-derived cells that are capable of contributing to re-endothelialization and neoangiogenesis.2 As levels of circulating EPCs independently predict the development and disease progression of atherosclerosis and have been linked to different pathologies associated with overweight, including hypertension, hypercholesterolemia, diabetes and coronary artery disease, it was important to investigate the influence of adiposity on EPCs in adults per se. MacEneaney et al. showed that circulating EPC numbers are lower in obese adults (body mass index (BMI) ⩾30 kg/m2), but not in overweight adults (BMI between 25 and 30 kg/m2), compared with normal weight adults (BMI < 25 kg/m2). As it is well established already that being overweight is associated with endothelial dysfunction and atheroslcerosis progression,3 it seems surprising that EPC counts are not lower, but higher (not significantly). In our study, we showed that being overweight influences EPCs in overweight adolescents, showing higher counts for CD34-negative EPCs.4 These results may indicate that the endogenous repair mechanism, ‘EPCs’, can adequately respond to, for example, low-grade vascular inflammation in moderately overweight adults and in overweight adolescents, but not in obese adults. Different studies proposed a limited pool of progenitor cells within the bone marrow,5 suggesting that being overweight has activated the bone marrow, leading to bone marrow failure after sustained activation. Oxidative stress, low-grade systemic inflammation and (adipo)cytokines have already been shown to contribute to the recruitment of EPCs. Originally, EPCs were defined as CD34+/VEGFR2+ or CD34+/CD133+/VEGFR2+ cells and recently, a CD34−/CD133+/VEGFR2+ population was discovered and identified to be much more sensitive to the environment.6 As mentioned, these cells were especially elevated in overweight teenagers. Unfortunately, this population was not tested in the paper by MacEneaney et al. Future research has to address different EPC subpopulations in overweight adults to understand regulatory mechanisms. A therapeutical conservation of endogenous repair capacities might help to positively influence adiposity-related cardiovascular risk for overweight and obese individuals.

The authors declare no conflict of interest.

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References

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Authors and Affiliations

  1. Clinic of Internal Medicine I, Friedrich-Schiller-University, Jena, Germany

    C Jung, M Fritzenwanger & H R Figulla

  2. Department of Medicine, Center for Molecular Medicine, Karolinska Institute, Stockholm, Sweden

    C Jung

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  1. C Jung
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  2. M Fritzenwanger
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  3. H R Figulla
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Correspondence to C Jung.

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Jung, C., Fritzenwanger, M. & Figulla, H. Endothelial progenitor cells in overweight: exhausted long before the summit?. Int J Obes 33, 702 (2009). https://doi.org/10.1038/ijo.2009.53

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