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. 2015 Apr 29;6:9. doi: 10.1186/s13293-015-0027-9

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© Ayaz and Howlett; licensee BioMed Central. 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Major gonadal pathways for testosterone biosynthesis. Gonadotropin-releasing hormone (GnRH) secreted from the hypothalamus releases luteinizing hormone (LH) from the pituitary. LH binds to LH receptors on Leydig cells, stimulates G_s, and activates the cAMP/protein kinase A (PKA) pathway. PKA promotes the transport of cholesterol into mitochondria and increases transcription of genes involved in testosterone biosynthesis. Cholesterol is converted to pregnenolone, which diffuses into the endoplasmic reticulum for testosterone biosynthesis via ∆⁴ and ∆⁵ pathways. Testosterone is formed by 17β-hydroxysteroid dehydrogenase 3 (HSD17β3) in the ∆⁴ pathway and by 3β-hydroxysteroid dehydrogenase (HSD3β) in the ∆⁵ pathway. Testosterone is converted to dihydrotestosterone (DHT) by 5α-reductase, and some are aromatized to 17ß-estradiol.