Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/95260
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Type: Journal article
Title: Insulin-like factor 3 and the HPG axis in the male
Author: Ivell, R.
Heng, K.
Anand-Ivell, R.
Citation: Frontiers in Endocrinology, 2014; 5(JAN):6-1-6-7
Publisher: Frontiers Media
Issue Date: 2014
ISSN: 1664-2392
1664-2392
Statement of
Responsibility: 
Richard Ivell, Kee Heng, and Ravinder Anand-Ivell
Abstract: The hypothalamic-pituitary-gonadal (HPG) axis comprises pulsatile GnRH from the hypothalamus impacting on the anterior pituitary to induce expression and release of both LH and FSH into the circulation. These in turn stimulate receptors on testicular Leydig and Sertoli cells, respectively, to promote steroidogenesis and spermatogenesis. Both Leydig and Sertoli cells exhibit negative feedback to the pituitary and/or hypothalamus via their products testosterone and inhibin B, respectively, thereby allowing tight regulation of the HPG axis. In particular, LH exerts both acute control on Leydig cells by influencing steroidogenic enzyme activity, as well as chronic control by impacting on Leydig cell differentiation and gene expression. Insulin-like peptide 3 (INSL3) represents an additional and different endpoint of the HPG axis. This Leydig cell hormone interacts with specific receptors, called RXFP2, on Leydig cells themselves to modulate steroidogenesis, and on male germ cells, probably to synergize with androgen-dependent Sertoli cell products to support spermatogenesis. Unlike testosterone, INSL3 is not acutely regulated by the HPG axis, but is a constitutive product of Leydig cells, which reflects their number and/or differentiation status and their ability therefore to produce various factors including steroids, together this is referred to as Leydig cell functional capacity. Because INSL3 is not subject to the acute episodic fluctuations inherent in the HPG axis itself, it serves as an excellent marker for Leydig cell differentiation and functional capacity, as in puberty, or in monitoring the treatment of hypogonadal patients, and at the same time buffering the HPG output.
Keywords: INSL3
RXFP2
Leydig cell
testosterone
puberty
hypothalamic hypogonadism
Rights: © 2014 Ivell, Heng and Anand-Ivell. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
DOI: 10.3389/fendo.2014.00006
Grant ID: http://purl.org/au-research/grants/nhmrc/1009243
Appears in Collections:Aurora harvest 7
Molecular and Biomedical Science publications

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