ArticleAsian journal of andrology
Reduced fetal androgen exposure compromises Leydig cell function in adulthood.
Article in Asian journal of andrology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 0 citations in OpenAlex.
- Leptin Receptor b (LEPRb) Mutations Disrupt Hypothalamic Control of the Reproductive Axis.International journal of molecular sciences · 2026Review
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disruption of normal fetal development can influence functioning of organs and cells in adulthood. Circumstantial evidence suggests that subtle reductions in fetal androgen production may be the cause of adult male reproductive disorders due to reduced testosterone production. The mechanisms through which these fetal events affect adult testosterone levels are largely unknown. A recent paper of Kilcoyne et al. provides evidence that fetal reduction in androgen production or signaling results in a reduced Leydig stems cell number after birth and concomitant Leydig cell failure in adulthood. This implies that fetal androgen deficiency can lead to negative programming of adult Leydig cell (ALC) function, which may have implications for general health, aging, and longevity.
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Registered trials
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