Editing Progesterone (section)

===Early sexual differentiation===
Progesterone plays a role in early human sexual differentiation.<ref name=wj>{{cite journal|doi=10.15347/WJM/2023.003  |doi-access=free |title=Alternative androgen pathways |year=2023 | vauthors = Masiutin M, Yadav M |journal=WikiJournal of Medicine |volume=10 |pages=X |s2cid=257943362}}</ref> [[Placenta]]l progesterone is the feedstock for the [[5α-dihydrotestosterone]] (DHT) produced via the [[Androgen backdoor pathway|backdoor pathway]] found operating in multiple non-gonadal tissues of the [[fetus]],<ref name="pmid30763313">{{cite journal | vauthors = O'Shaughnessy PJ, Antignac JP, Le Bizec B, Morvan ML, Svechnikov K, Söder O, Savchuk I, Monteiro A, Soffientini U, Johnston ZC, Bellingham M, Hough D, Walker N, Filis P, Fowler PA | display-authors = 6 | title = Alternative (backdoor) androgen production and masculinization in the human fetus | journal = PLOS Biology | volume = 17 | issue = 2 | pages = e3000002 | date = February 2019 | pmid = 30763313 | pmc = 6375548 | doi = 10.1371/journal.pbio.3000002 | doi-access = free }}</ref> whereas deficiencies in this pathway lead to undervirilization of the male fetus, resulting in incomplete development of the male genitalia.<ref name="pmid24793988">{{cite journal | vauthors = Flück CE, Pandey AV | title = Steroidogenesis of the testis -- new genes and pathways | journal = Annales d'Endocrinologie | volume = 75 | issue = 2 | pages = 40–47 | date = May 2014 | pmid = 24793988 | doi = 10.1016/j.ando.2014.03.002 }}</ref><ref name="pmid8636249">{{cite journal | vauthors = Zachmann M | title = Prismatic cases: 17,20-desmolase (17,20-lyase) deficiency | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 81 | issue = 2 | pages = 457–459 | date = February 1996 | pmid = 8636249 | doi = 10.1210/jcem.81.2.8636249 | doi-access = free }}</ref> DHT is a potent [[androgen]] that is responsible for the development of male genitalia, including the [[penis]] and [[scrotum]].{{cn|date=February 2025}}

During early fetal development, the undifferentiated gonads can develop into either testes or ovaries. The presence of the [[Y chromosome]] leads to the development of testes. The testes then produce testosterone, which is converted to DHT via the enzyme [[5α-Reductase|5α-reductase]]. DHT is a potent androgen that is responsible for the masculinization of the external genitalia and the development of the prostate gland. Progesterone, produced by the placenta during pregnancy, plays a role in fetal sexual differentiation by serving as a precursor molecule for the synthesis of DHT via the backdoor pathway. In the absence of adequate levels of [[steroidogenic enzymes]] during fetal development, the [[Androgen backdoor pathway#Dihydrotestosterone backdoor biosynthesis|backdoor pathway for DHT synthesis]] can become deficient, leading to undermasculinization of the male fetus. This can result in the development of ambiguous genitalia or even female genitalia in some cases. Therefore, both DHT and progesterone play crucial roles in early fetal sexual differentiation, with progesterone acting as a precursor molecule for DHT synthesis and DHT promoting the development of male genitalia.<ref name=wj/>