Format

Send to

Choose Destination
Cell Metab. 2014 Dec 2;20(6):1049-58. doi: 10.1016/j.cmet.2014.10.010. Epub 2014 Nov 20.

Loss of white adipose hyperplastic potential is associated with enhanced susceptibility to insulin resistance.

Author information

1
Department of Medicine, Division of Genetics, Brigham and Women's Hospital, Boston, MA 02115, USA.
2
National Resource for Imaging Mass Spectroscopy, Brigham and Women's Hospital, Cambridge, MA 02138, USA.
3
Department of Medicine, Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA.
4
Department of Medicine, Division of Genetics, Brigham and Women's Hospital, Boston, MA 02115, USA; National Resource for Imaging Mass Spectroscopy, Brigham and Women's Hospital, Cambridge, MA 02138, USA; Harvard Medical School, Boston, MA 02115, USA.
5
Department of Medicine, Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA.
6
Department of Medicine, Division of Genetics, Brigham and Women's Hospital, Boston, MA 02115, USA; Department of Medicine, Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Harvard Stem Cell Institute, Cambridge, MA 02138, USA. Electronic address: msteinhauser@partners.org.

Abstract

Fat mass expansion occurs by adipocyte hypertrophy or recruitment of differentiating adipocyte progenitors, the relative balance of which may impact systemic metabolism. We measured adipogenesis in murine subcutaneous (sWAT) and visceral white adipose tissue (vWAT) using stable isotope methodology and then modeled adipocyte turnover. Birth and death rates were similar within depots; however, turnover was higher in vWAT relative to sWAT. In juvenile mice, obesity increased adipogenesis, but in adults, this was only seen in vWAT after prolonged high-fat feeding. Statistical modeling suggests differentiation of adipocyte progenitors without an accompanying self-renewing division step may partially explain the age-dependent decline in hyperplastic potential. Additional metabolic interrogation of obese mice demonstrated an association between adipocyte turnover and insulin sensitivity. These data therefore identify adipocyte hypertrophy as the dominant mechanism of adult fat mass expansion and support the paradoxical concept that metabolic disease ensues due to a failure of adipose tissue plasticity.

PMID:
25456741
PMCID:
PMC4715375
DOI:
10.1016/j.cmet.2014.10.010
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center