Aging
Navigate
Submit an Article
Research Paper|Volume 6, Issue 7|pp 575—586

Growth hormone action predicts age-related white adipose tissue dysfunction and senescent cell burden in mice

Michael B. Stout1, Tamara Tchkonia1, Tamar Pirtskhalava1, Allyson K. Palmer1, Edward O. List2, Darlene E. Berryman2, Ellen R. Lubbers2, Carlos Escande1, Adam Spong3, Michal M. Masternak4, Ann L. Oberg5, Nathan K. LeBrasseur1, Richard A. Miller6, John J. Kopchick2, Andrzej Bartke3, James L. Kirkland1
  • 1Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN 55905, USA
  • 2Edison Biotechnology Institute and Heritage College of Osteopathic Medicine, Ohio University, Athens, OH 45701, USA
  • 3Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL 62794, USA
  • 4Burnett School of Biomedical Sciences, University of Central Florida, Orlando, FL 32827, USA
  • 5Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN 55905, USA
  • 6Department of Pathology and Geriatrics Center, University of Michigan, Ann Arbor, MI 48109, USA

* * Equal contribution

Received: June 2, 2014Accepted: July 17, 2014Published: July 20, 2014
https://doi.org/10.18632/aging.100681

Copyright: © 2014 Stout et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The aging process is associated with the development of several chronic diseases. White adipose tissue (WAT) may play a central role in age-related disease onset and progression due to declines in adipogenesis with advancing age. Recent reports indicate that the accumulation of senescent progenitor cells may be involved in age-related WAT dysfunction. Growth hormone (GH) action has profound effects on adiposity and metabolism and is known to influence lifespan. In the present study we tested the hypothesis that GH activity would predict age-related WAT dysfunction and accumulation of senescent cells. We found that long-lived GH-deficient and -resistant mice have reduced age-related lipid redistribution. Primary preadipocytes from GH-resistant mice also were found to have greater differentiation capacity at 20 months of age when compared to controls. GH activity was also found to be positively associated with senescent cell accumulation in WAT. Our results demonstrate an association between GH activity, age-related WAT dysfunction, and WAT senescent cell accumulation in mice. Further studies are needed to determine if GH is directly inducing cellular senescence in WAT or if GH actions on other target organs or alternative downstream alterations in insulin-like growth factor-1, insulin or glucose levels are responsible.