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A mediator of metabolic signals influences puberty and growth

Variants of the melanocortin 3 receptor are associated with delayed puberty and reduced growth, suggesting that this receptor might integrate signals of metabolic status that affect body growth and sexual maturation.
  1. Alejandro Lomniczi

    1. Alejandro Lomniczi is in the Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon 97006, USA.

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Body growth and the onset of puberty are regulated by neurons located in a part of the brain called the hypothalamus. In the central hypothalamus, signalling by hormones called melanocortins relays metabolic information to downstream growth and reproductive centres. However, the molecular and cellular targets of these signals have not been completely elucidated. Writing in Nature, Lam et al.1 describe previously unreported mutations in the gene encoding the human melanocortin 3 receptor (MC3R) protein that seem to disrupt the receptor’s function. They found that these mutations are associated with a delay in the onset of puberty as well as with reduced childhood growth, adult height and lean body mass.

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Nature 599, 377-379 (2021)

doi: https://doi.org/10.1038/d41586-021-02954-0

References

  1. Lam, B. Y. H. et al. Nature 599, 436–441 (2021).

    Article  Google Scholar 

  2. Kennedy, G. C. J. Endocrinol. 16, 9–17 (1957).

    Article  PubMed  Google Scholar 

  3. Kennedy, G. C. & Mitra, J. J. Physiol. (Lond.) 166, 408–418 (1963).

    Article  Google Scholar 

  4. Hill, J. W. & Faulkner, L. D. Neuroendocrinology 104, 330–346 (2017).

    Article  PubMed  Google Scholar 

  5. Chen, A. S. et al. Transgenic Res. 9, 145–154 (2000).

    Article  PubMed  Google Scholar 

  6. Vaisse, C., Clement, K., Guy-Grand, B. & Froguel, P. Nature Genet. 20, 113–114 (1998).

    Article  PubMed  Google Scholar 

  7. Farooqi, I. S. et al. N. Engl. J. Med. 348, 1085–1095 (2003).

    Article  PubMed  Google Scholar 

  8. Chen, A. S. et al. Nature Genet. 26, 97–102 (2000).

    Article  PubMed  Google Scholar 

  9. Uenoyama, Y. et al. Front. Endocrinol. 10, 312 (2019).

    Article  Google Scholar 

  10. Steyn, F. J., Tolle, V., Chen, C. & Epelbaum, J. Compr. Physiol. 6, 687–735 (2016).

    Article  PubMed  Google Scholar 

  11. Hauspie, R. C., Vercauteren, M. & Susanne, C. Acta Paediatr. 86 (Suppl. 423), 20–27 (1997).

    Article  Google Scholar 

Download references

Competing Interests

The author declares no competing interests.

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