Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • NEWS AND VIEWS

Unexpected cell population gives fat a brake

Single-cell transcriptional profiling of stem and progenitor cells in fat tissue identifies distinct cell subpopulations, one of which inhibits fat growth by signalling to neighbouring cells.
  1. David A. Guertin

    1. David A. Guertin is at the University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.

    View author publications

    You can also search for this author in PubMed  Google Scholar

Fat tissue has a remarkable capacity for growth. It can expand in two ways: by increasing the size of individual fat cells (adipocytes), and by making adipocytes from progenitor cells through the process of adipogenesis. Fat is essential for metabolic fitness, but having too much fat in the wrong places can be harmful. Obesity is a precursor to serious medical conditions such as type 2 diabetes, cardiovascular disease and cancer, which are ravaging health-care systems worldwide. Key to combating obesity is understanding how mature adipocytes develop from precursor cells, but the identity of these precursors has so far been elusive. In a paper in Nature, Schwalie et al.1 define three populations of fat-precursor cell, one of which unexpectedly functions to suppress adipocyte production.

Access options

Rent or buy this article

Prices vary by article type

from$1.95

to$39.95

Learn more

Prices may be subject to local taxes which are calculated during checkout

Nature 559, 41-42 (2018)

doi: https://doi.org/10.1038/d41586-018-05120-1

References

  1. Schwalie, P. C. et al. Nature 559, 103–108 (2018).

    Article  Google Scholar 

  2. Sanchez-Gurmaches, J., Hung, C.-M. & Guertin, D. A. Trends Cell Biol. 26, 313–326 (2016).

    Article  PubMed  CAS  Google Scholar 

  3. Lynes, M. D. & Tseng, Y.-H. Ann. NY Acad. Sci. 1411, 5–20 (2018).

    Article  PubMed  Google Scholar 

  4. Schoettl, T., Fischer, I. P. & Ussar, S. J. Exp. Biol. 221, jeb162958 (2018).

    Article  PubMed  Google Scholar 

  5. Rosen, E. D. & Spiegelman, B. M. Cell 156, 20–44 (2014).

    Article  PubMed  CAS  Google Scholar 

  6. Hepler, C., Vishvanath, L. & Gupta, R. K. Genes Dev. 31, 127–140 (2017).

    Article  PubMed  CAS  Google Scholar 

  7. Berry, R., Jeffery, E. & Rodeheffer, M. S. Cell Metab. 19, 8–20 (2014).

    Article  PubMed  CAS  Google Scholar 

  8. Tang, W. et al. Science 322, 583–586 (2008).

    Article  PubMed  CAS  Google Scholar 

  9. Orkin, S. H. & Zon, L. I. Cell 132, 631–644 (2008).

    Article  PubMed  CAS  Google Scholar 

  10. Kusuma, G. D., Carthew, J., Lim, R. & Frith, J. E. Stem Cells Dev. 26, 617–631 (2017).

    Article  PubMed  CAS  Google Scholar 

Download references

Subjects

Latest on:

Nature Careers

Jobs

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing

Search

Advanced search

Quick links