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Effects of the insulin‐like growth factor system on testicular differentiation and function: a review of the literature
Author(s) -
Cannarella R.,
Condorelli R. A.,
La Vignera S.,
Calogero A. E.
Publication year - 2018
Publication title -
andrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.947
H-Index - 43
eISSN - 2047-2927
pISSN - 2047-2919
DOI - 10.1111/andr.12444
Subject(s) - insulin like growth factor 1 receptor , sertoli cell , pi3k/akt/mtor pathway , biology , endocrinology , growth factor , medicine , insulin like growth factor , protein kinase b , follicle stimulating hormone receptor , receptor , signal transduction , follicle stimulating hormone , hormone , microbiology and biotechnology , spermatogenesis , genetics , luteinizing hormone
Summary We recently described the occurrence of cryptorchidism, oligoasthenoteratozoospermia, and genital abnormalities in patients with distal 15q chromosome structural abnormalities. This observation brought us to hypothesize that insulin‐like growth factor ( IGF ) receptor ( IGF 1R ), mapping on the 15q 26.3 chromosomal band, may be involved in testicular function. To further evaluate this topic, we reviewed in vitro and in vivo studies exploring the role of the IGF system [ IGF 1, IGF 2, IGF 1R, insulin receptor substrates ( IRS )] at the testicular level both in animals and in humans. In animals, IGF 1/ IGF 1R has been found to be involved in testicular development during embryogenesis, in Sertoli cell ( SC ) proliferation, and in germ cell ( GS ) proliferation and differentiation. Interestingly, IGF 1R seems to mediate follicle‐stimulating hormone ( FSH ) effects through the PI 3K/ AKT pathway. In humans, IGF 1 directly increases testicular volume. The molecular pathways responsible for testicular differentiation and IGF 1/ IGF 1R signaling are highly conserved among species; therefore, the IGF system may be involved in FSH signaling also in humans. We suggest a possible molecular pathway occurring in human SC s, which involves both IGF 1 and FSH through the PI 3K/ AKT pathway. The acknowledgment of an IGF 1 mediation of the FSH ‐induced effects may open new ways for a targeted therapy in idiopathic non‐ FSH ‐responder oligoasthenoteratozoospermia.