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Effects of an Igf1 Gene Null Mutation on Mouse Reproduction
Open accessAbstract
Both sexes of adult mice homozygous for a targeted mutation of the Igf1 gene, encoding insulin-like growth factor 1, are infertile dwarfs (approximately 30% of normal size). The testes are reduced in size less than expected from the degree of dwarfism but sustain spermatogenesis only at 18% of the normal level. The epididymides are overall nearly allometric to the reduced body weight, but the distal regions of the duct, vas deferens, seminal vesicles, and prostate are vestigial. Despite the mutational impact on the epididymis, capacitated sperm are able to fertilize wild type eggs in vitro. It is hypothesized that the infertility of male mutants is caused by failure of androgenization resulting in absence of mating behavior, due to drastically reduced levels of serum testosterone (18% of normal). This hormonal deficiency was correlated with an ultrastructural analysis of mutant Leydig cells revealing a significant developmental delay, while assays in organ culture showed that the basal and LH-stimulated production of testosterone by testicular parenchyma is reduced in comparison with wild type controls. The female mutants fail to ovulate even after administration of gonadotropins, which is apparently the primary cause of their infertility, and possess an infantile uterus that exhibits a dramatic hypoplasia especially in the myometrium. The phenotypic manifestations of the mutation were correlated with the localization of transcripts for insulin-like growth factor I and its cognate receptor in wild type reproductive tissues by in situ hybridization.
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“In IGF-1 gene null, –/– mutant mice (10), the testes, epididymides duct, vas deferens, seminal vesicles, and prostate are vestigial, leading to a low spermatogenesis rate at 18% of the normal level.”
From Growth Hormone Is Beneficial for Induction of Spermatogenesis in Adult Patients With Congenital Combined Pituitary Hormone Deficiency (2022) · cites this paper as [10]
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Metadata
- Authors
- Baker, J., Hardy, M. P., Zhou, J., Bondy, C., Lupu, F., Bellvé, A. R., & Efstratiadis, A.
- Affiliations
- Columbia University (US)
- Venue
- Molecular Endocrinology
- Publisher
- The Endocrine Society
- Published
- 1996-07
- Volume
- 10
- Issue
- 7
- Pages
- 903-918
- ISSN
- 0888-8809 (ISSN-L)
- 1944-9917
- OpenAlex
- W2065752045
- Cited by
- 674
- References
- 45
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 11 · 2023: 18 · 2022: 19 · 2021: 24 · 2020: 29 · 2019: 20 · 2018: 29 · 2017: 19 · 2016: 20 · 2015: 20 · 2014: 23 · 2013: 23 · 2012: 16
- FWCI
- 19.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01hd029010-03, 5r01hd028342-04)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-29010, HD-28342, HD32588)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- insulin-like growth factor I, male infertility, dwarfism, spermatogenesis, Leydig cell development, androgen deficiency, androgenization, epididymis, female infertility, ovulation, myometrium, gonadotropin resistance, IGF-1 receptor, reproductive tract development
- MeSH terms
- Animals, Epididymis, Female, Infertility, Insulin-Like Growth Factor I, Male, Mice, Mutant Strains, Mutation, Organ Size, Ovary, Reproduction, Sperm Motility, Testis, Testosterone, Uterus, Gene Expression Regulation, Developmental, Mice
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