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.

  • Brief Communication
  • Published:

Pomc-expressing progenitors give rise to antagonistic neuronal populations in hypothalamic feeding circuits

Nature Medicine volume 16, pages 403–405 (2010)Cite this article

Subjects

Abstract

Hypothalamic neuron circuits regulating energy balance are highly plastic and develop in response to nutrient and hormonal cues. To identify processes that might be susceptible to gestational influences in mice, we characterized the ontogeny of proopiomelanocortin (POMC) and neuropeptide Y (NPY) cell populations, which exert opposing influences on food intake and body weight. These analyses revealed that Pomc is broadly expressed in immature hypothalamic neurons and that half of embryonic Pomc-expressing precursors subsequently adopt a non-POMC fate in adult mice. Moreover, nearly one quarter of the mature NPY+ cell population shares a common progenitor with POMC+ cells.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

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

Figure 1: Pomc is transiently expressed in a broad population of hypothalamic neurons during embryonic development.
Figure 2: NPY neurons derived from a Pomc-expressing lineage persist to adulthood.

Similar content being viewed by others

References

  1. Ogden, C.L. et al. J. Am. Med. Assoc. 295, 1549–1555 (2006).

    Article  CAS  Google Scholar 

  2. Taylor, P.D. & Poston, L. Exp. Physiol. 92, 287–298 (2007).

    Article  CAS  Google Scholar 

  3. Levin, B.E. Phil. Trans. R. Soc. Lond. B 361, 1107–1121 (2006).

    Article  CAS  Google Scholar 

  4. Bouret, S.G., Draper, S.J. & Simerly, R.B. Science 304, 108–110 (2004).

    Article  CAS  Google Scholar 

  5. Shankar, K. et al. Am. J. Physiol. Regul. Integr. Comp. Physiol. 294, R528–R538 (2008).

    Article  CAS  Google Scholar 

  6. Saper, C.B., Chou, T.C. & Elmquist, J.K. Neuron 36, 199–211 (2002).

    Article  CAS  Google Scholar 

  7. Cowley, M.A. et al. Nature 411, 480–484 (2001).

    Article  CAS  Google Scholar 

  8. Ollmann, M.M. et al. Science 278, 135–138 (1997).

    Article  CAS  Google Scholar 

  9. Schwartz, M.W. & Porte, D. Jr. Science 307, 375–379 (2005).

    Article  CAS  Google Scholar 

  10. Altman, J. & Bayer, S.A. J. Comp. Neurol. 182, 945–971 (1978).

    Article  CAS  Google Scholar 

  11. Shimada, M. & Nakamura, T. Exp. Neurol. 41, 163–173 (1973).

    Article  CAS  Google Scholar 

  12. Broad, K.D., Curley, J.P. & Keverne, E.B. Dev. Neurobiol. 69, 314–325 (2009).

    Article  CAS  Google Scholar 

  13. Cottrell, E.C. et al. Am. J. Physiol. Regul. Integr. Comp. Physiol. 296, R631–R639 (2009).

    Article  CAS  Google Scholar 

  14. Nilsson, I., Johansen, J.E., Schalling, M., Hokfelt, T. & Fetissov, S.O. Brain Res. Dev. Brain Res. 155, 147–154 (2005).

    Article  CAS  Google Scholar 

  15. Pinto, S. et al. Science 304, 110–115 (2004).

    Article  CAS  Google Scholar 

  16. van den Top, M. et al. Neuroscience 144, 815–824 (2007).

    Article  CAS  Google Scholar 

  17. Zinyk, D.L., Mercer, E.H., Harris, E., Anderson, D.J. & Joyner, A.L. Curr. Biol. 8, 665–668 (1998).

    Article  CAS  Google Scholar 

  18. Balthasar, N. et al. Neuron 42, 983–991 (2004).

    Article  CAS  Google Scholar 

  19. Fioramonti, X. et al. Diabetes 56, 1219–1227 (2007).

    Article  CAS  Google Scholar 

  20. Chen, H., Simar, D., Lambert, K., Mercier, J. & Morris, M.J. Endocrinology 5348–56 (2008).

Download references

Acknowledgements

We thank L. Sussel, H. Wichterle and D. Accili for critical reading of our manuscript and helpful comments; R. Leibel for support and major funding for this project (RO1 DK52431-16); J. Overton for help with confocal imaging; L. Yang of the Diabetes and Endocrinology Research Center Pathology Core for cryosectioning and C. Liu of the Irving Institute Clinical and Translational Science Award, FACS core (National Center for Research Resources UL1 RR024156); M. Low for Pomc-GFP mice (University of Michigan Health Center), J. Elmquist for Pomc-Cre mice (Univerisity of Texas Southwestern Medical Center) and B. Lowell for Npy-hrGFP mice (Beth Israel Deaconess Medical Center) for generously providing mouse reagents. This work was supported by F31DK079372 (S.L.P.), US Institute of Human Nutrition Training Grant 2T32DK007647-21 (J.S.C.), American Diabetes Association Grant 7-07RA-195 (L.M.Z.), Columbia Diabetes and Endocrinology Research Center Pilot and Feasibility Award P30 DK63608-07 (L.M.Z.) and NY Obesity Research Center Pilot and Feasibility Grant P30 DK26687-26 (L.M.Z.).

Author information

Authors and Affiliations

  1. Institute of Human Nutrition, Columbia University, New York, New York, USA

    Stephanie L Padilla & Jill S Carmody

  2. Naomi Berrie Diabetes Center, Columbia University, New York, New York, USA

    Stephanie L Padilla, Jill S Carmody & Lori M Zeltser

  3. Department of Pathology and Cell Biology, Columbia University, New York, New York, USA

    Lori M Zeltser

Authors
  1. Stephanie L Padilla
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Jill S Carmody
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Lori M Zeltser
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

S.L.P. performed experiments, analyzed data and wrote the paper; J.S.C. generated data for confocal analysis and contributed to data analysis; L.M.Z. designed the study, analyzed the data and wrote the paper.

Corresponding author

Correspondence to Lori M Zeltser.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Supplementary information

Supplementary Text and Figures

Supplementary Figures 1–6 and Supplementary Methods (PDF 389 kb)

Rights and permissions

Reprints and permissions

About this article

Cite this article

Padilla, S., Carmody, J. & Zeltser, L. Pomc-expressing progenitors give rise to antagonistic neuronal populations in hypothalamic feeding circuits. Nat Med 16, 403–405 (2010). https://doi.org/10.1038/nm.2126

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nm.2126

This article is cited by

Search

Advanced search

Quick links

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