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INSL3 as a biomarker of Leydig cell functionality

Ivell, Richard; Wade, John D.; Anand-Ivell, Ravinder

Authors

Richard Ivell

John D. Wade

Ravinder Anand-Ivell



Abstract

Insulin-like factor 3 (INSL3) is a small peptide hormone made and secreted uniquely by mature Leydig cells in the testes of all mammals. Importantly, this expression and secretion appears to be constitutive and therefore reflects the differentiation status and number of the Leydig cells present, differing thereby from testosterone, which is acutely and homeostatically regulated by the hormones of the hypothalamic-pituitary-gonadal axis. As a consequence, the measurement of INSL3 either as mRNA in the testis or as secreted peptide circulating in the blood provides an excellent assessment of Leydig cell differentiation, for example, during fetal development, puberty, or aging or following exposure to endocrine-disrupting agents. Whereas INSL3 is proving increasingly useful as a biomarker for testis status, less is known about its functions, particularly in the adult male. Current evidence points to autocrine, paracrine, and endocrine roles, acting through the G-protein-coupled receptor called RXFP2, although more research is required to characterize these functions in detail.

Journal Article Type Article
Publication Date Jun 1, 2013
Journal Biology of Reproduction
Print ISSN 0006-3363
Electronic ISSN 1529-7268
Publisher Oxford University Press (OUP)
Peer Reviewed Peer Reviewed
Volume 88
Issue 6
Institution Citation Ivell, R., Wade, J. D., & Anand-Ivell, R. (2013). INSL3 as a biomarker of Leydig cell functionality. Biology of Reproduction, 88(6), doi:10.1095/biolreprod.113.108969
DOI https://doi.org/10.1095/biolreprod.113.108969
Keywords HPG axis, hypogonadism, INSL3, Leydig cell, puberty, testosterone
Publisher URL https://academic.oup.com/biolreprod/article-lookup/doi/10.1095/biolreprod.113.108969
Copyright Statement Copyright information regarding this work can be found at the following address: http://eprints.nottingh.../end_user_agreement.pdf

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Copyright Statement
Copyright information regarding this work can be found at the following address: http://eprints.nottingham.ac.uk/end_user_agreement.pdf





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