Consequences of steroid-5α-reductase deficiency and inhibition in vertebrates.
Level 5 - mechanism / opinion, no new human data
Narrative review of comparative vertebrate biology and mechanism-based reasoning with no systematic search methodology.
PubMed 31981690 · doi:10.1016/j.ygcen.2020.113400
What was done
This narrative review summarizes comparative vertebrate literature on the morphological, physiological, and molecular effects of steroid-5α-reductase (SRD5α) deficiency resulting from genetic mutations or pharmacological inhibitors (such as finasteride and dutasteride).
What was found
The abstract reports no numerical data or effect estimates. It outlines key roles for SRD5α isozymes across species: SRD5α2 and 5α-dihydrotestosterone (5α-DHT) in male secondary sexual differentiation and non-mammalian sex determination; SRD5α1 in synthesizing neurosteroids (allopregnanolone and 3α-diol) involved in anxiety and sexual behavior; and SRD5α3 in N-glycosylation. It also notes SRD5α involvement in uterine steroid degradation during pregnancy, hepatic glucocorticoid clearance, and transcriptional/epigenetic regulation via hormone receptors and DNA methylation.
Why it matters
Understanding the broad comparative biology of SRD5α isozymes provides mechanistic context for the systemic and non-androgenic physiological consequences of therapeutic 5α-reductase inhibitors.
Limits
The abstract describes a broad narrative synthesis without defined systematic search criteria, quality appraisal of included studies, or quantitative human outcome data.
Cited by
- supports Dihydrotestosterone (DHT) is the most potent androgenic hormone in the human body.