Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 371, Issue 1-2, Pages 124-132Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2013.01.017
Keywords
Androgens; Aldo-keto reductase: gonad; Steroidogenesis; Genital development
Categories
Funding
- Swiss National Science Foundation [31003A-130710, 31003A-134926, 320000-130645]
- National Institutes of Health [DK37922]
- Swiss National Science Foundation (SNF) [31003A_130710] Funding Source: Swiss National Science Foundation (SNF)
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Following development of the fetal bipotential gonad into a testis, male genital differentiation requires testicular androgens. Fetal Leydig cells produce testosterone that is converted to dihydrotestosterone in genital skin, resulting in labio-scrotal fusion. An alternative 'backdoor' pathway of dihydrotestosterone synthesis that bypasses testosterone has been described in marsupials, but its relevance to human biology has been uncertain. The classic and backdoor pathways share many enzymes, but a 3 alpha-reductase, AKR1C2, is unique to the backdoor pathway. Human AKR1C2 mutations cause disordered sexual differentiation, lending weight to the idea that both pathways are required for normal human male genital development. These observations indicate that fetal dihydrotestosterone acts both as a hormone and as a paracrine factor, substantially revising the classic paradigm for fetal male sexual development. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
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