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Cited by 674Growth Hormone and Insulin-like Growth FactorsSperm and Testicular FunctionHypothalamic control of reproductive hormones

Effects of an Igf1 Gene Null Mutation on Mouse Reproduction

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Baker, J, Hardy, M P, Zhou, J, Bondy, C, Lupu, F, Bellvé, A R, Efstratiadis, A·1996·Molecular Endocrinology
DOI 10.1210/mend.10.7.8813730
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Abstract

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, the testes, epididymides duct, vas deferens, seminal vesicles, and prostate are vestigial, leading to a spermatogenesis rate at 18% of the normal level.

    “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]

    The Reproductive section (page not provided) describes vestigial seminal vesicles, a severely reduced prostate and vas deferens, and sperm numbers in the testis and epididymis averaging about 17–18% of normal. It does not describe the testes or entire epididymal duct as vestigial: testicular weight was 41% of normal, and epididymal weight was nearly proportional to body size. The 18% figure measures sperm number, not spermatogenesis rate, and the paper does not establish that organ size caused that reduction. (LLM, conf=0.90)

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Research works printed but not linked: 5

  1. Scanes CG, Daughaday WH 1995 Growth hormone action: growth. In: Harvey S, Scanes CG, Daughaday WH (eds) Growth Hormone. CRC Press, Boca Raton, FL, pp 351-369
  2. Adashi EY 1993 The intraovarian insulin-like growth fac- tor system. In: Adashi EY, Leung PCK (eds) The Ovary. Raven Press, New York, pp 319-335
  3. Magoffin DA, Erickson GF 1994 Control systems of theta-interstitial cells. In: Findlay JK (ed) Molecular Bi- ology of the Female Reproductive System. Academic Press, New York, pp 39-65
  4. van Buul-Offers S 1983 Hormonal and other inherited growth disturbances in mice with special reference to the Snell dwarf mouse. A review. Acta Endocrinol (Copenh) 103:1-47
  5. Camper SA, Saunders TL, Katz RW, Reeves RH 1990 The Pit-l transcription factor gene is a candidate for the murine Snell dwarf mutation. Genomics 8:586-590

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Authors
Baker, J., Hardy, M. P., Zhou, J., Bondy, C., Lupu, F., Bellvé, A. R., & Efstratiadis, A.
Affiliations
Columbia University (US)
ORCID
Venue
Molecular Endocrinology
Publisher
The Endocrine Society
Published
1996-07
Volume
10
Issue
7
Pages
903-918
ISSN
  • 0888-8809 (ISSN-L)
  • 1944-9917
DOI
10.1210/mend.10.7.8813730
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
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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