Testicular steroidogenesis in the testicular feminized ( Tfm ) mouse: loss of 17α-hydroxylase activity
Abstract
Testicular feminized (Tfm) mice are totally insensitive to androgen and may be used to study the role of the androgen receptor in normal development and function. We have examined testicular and Leydig cell steroidogenesis in Tfm mice. Serum bioactive LH was high in Tfm mice but serum testosterone was low and this was associated with a severe reduction in testicular testosterone production in vitro. Examination of [3H]pregnenolone metabolism by testes of Tfm mice indicated that progesterone, rather than testosterone, was the major steroid produced. Leydig cells were isolated from normal and Tfm mice and from normal mice in which testicular descent was surgically prevented before puberty. As in whole testes, androgen production in response to human chorionic gonadotrophin was severely reduced in Leydig cells from testes of Tfm mice compared with normal or cryptorchid groups. In contrast, progesterone production by Leydig cells from testes of Tfm mice was markedly increased in comparison with other groups. Total steroid production (progesterone plus androstenedione plus testosterone), however, was only 24% of normal in Leydig cells from Tfm mice. The pattern of steroid production by Leydig cells from cryptorchid testes was similar to control, although total steroid production was reduced to about 50% (this was significantly higher than the Tfm group, P<0·05). The high progesterone/androgen ratio in testes from Tfm mice suggested that 17α-hydroxylase was depleted in these animals. To confirm this, activity of the four major steroidogenic enzymes associated with the smooth endoplasmic reticulum was measured. Activities (per testis) of 3β-hydroxysteroid dehydrogenase and 5α-reductase were normal in Tfm and cryptorchid mice but, as expected, 17α-hydroxylase activity was only 2·4% of control and 4·5% of cryptorchid testes. 17-Ketosteroid reductase activity was markedly reduced in cryptorchid testes (14·4% of control) but there was a further reduction in testes from Tfm mice to 0·1% of control. Results show that the Tfm mutation is associated with marked loss of 17α-hydroxylase and 17-ketosteroid reductase activities. This suggests that these enzymes may require receptor-mediated androgen stimulation during development to express normal activity. Journal of Endocrinology (1991) 131, 443–449
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Tfm mice have reduced endogenous testosterone levels and develop hepatic steatosis as well as aortic fatty streaks when fed a HFD.
“Tfm mice have reduced endogenous testosterone levels 129 and develop hepatic steatosis as well as aortic fatty streaks when fed a HFD.”
From The role of the androgen receptor in the pathogenesis of obesity and its utility as a target for obesity treatments (2022) · cites this paper as [129]
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- Authors
- Murphy, L., & O'Shaughnessy, P. J.
- Affiliations
- Royal Veterinary College (GB)
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- Published
- 1991-12-01
- Volume
- 131
- Issue
- 3
- Pages
- 443-449
- ISSN
- 0022-0795 (ISSN-L)
- 1479-6805
- OpenAlex
- W1977053579
- Cited by
- 80
- References
- 0
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 1 · 2022: 5 · 2021: 4 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 6 · 2016: 3 · 2014: 4 · 2013: 2 · 2012: 1
- FWCI
- 0.13
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sexual Differentiation and Disorders
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal and reproductive studies
- Keywords
- 17α-hydroxylase, Leydig cells, steroidogenesis, androgen insensitivity syndrome, androgen receptor, cryptorchidism, progesterone secretion, testosterone production, 3β-hydroxysteroid dehydrogenase, 5α-reductase
- MeSH terms
- Androgens, Androstenedione, Animals, Cells, Cultured, Cryptorchidism, Leydig Cells, Luteinizing Hormone, Male, Mice, Mutant Strains, Progesterone, Steroid 17-alpha-Hydroxylase, Androgen-Insensitivity Syndrome, Testis, Testosterone, 17-Hydroxysteroid Dehydrogenases, Mice
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