The DOI matches its Crossref record; 148 of the 149 references it cites were found in a registry or an index.
The Consequences of Altered Somatotropic System on Reproduction1
Abstract
Although the primary control of gonadotropin secretion is by the hypothalamic GnRH and the gonadal function is controlled by the pituitary gonadotropins and prolactin, the emerging evidence suggests a vital role of the somatotropic axis, growth hormone (GH), and insulin-like growth factor-I (IGF-I) in the control of the pituitary and gonadal functions. It has been shown that GH deficiency, GH resistance, and experimental alterations in IGF-I secretion modify folliculogenesis, ovarian maturation, ovulation, and pregnancy, and in the male, GH/IGF-I plays an important role in spermatogenesis and the Leydig cell function. The primary focus of this review is to examine the role of GH/ IGF-I on the onset of puberty, fertility, pituitary, and gonadal endocrine functions. A number of studies have revealed that fertility is affected in GH-deficient dwarf and in IGF-I gene-ablated mice, possibly due to subnormal function of either the pituitary gland or the gonads. In the female GH receptor gene knockout (GHR-KO) mice, there was impairment in follicular development, ovulation rate, sexual maturation, production of and responsiveness to pheromonal signals, and the corpus luteum function. In IGF-I-deficient male GHR-KO mice, puberty is delayed, spermatogenesis is affected, and neuroendocrine-gonadal function is attenuated. Similarly, in some of the human Laron syndrome patients, puberty is delayed due to GH resistance. These data suggest that, in addition to GnRH and gonadotropins, GH/IGF-I influences the pituitary and gonadal functions in animals and humans.
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“Indeed, the growth hormone/insulin-like growth factor 1 (GH/IGF-1) and the hypothalamic-pituitary-gonadal (HPG) axes are closely interconnected (8).”
From Growth Hormone Is Beneficial for Induction of Spermatogenesis in Adult Patients With Congenital Combined Pituitary Hormone Deficiency (2022) · cites this paper as [8]
Citations
Cites
IGF-1 receptor regulates lifespan and resistance to oxidative stress in mice
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Cited by
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Life Extension in the Dwarf Mouse
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Metadata
- Authors
- Chandrashekar, V., Zaczek, D., & Bartke, A.
- Affiliations
- Southern Illinois University Carbondale (US)
- ORCID
- Bartke, Andrzej
- Venue
- Biology of Reproduction
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-07-01
- Volume
- 71
- Issue
- 1
- Pages
- 17-27
- ISSN
- 0006-3363 (ISSN-L)
- 1529-7268
- OpenAlex
- W2066929307
- Cited by
- 175
- References
- 149
- Citations by year
- 2026: 3 · 2024: 4 · 2023: 4 · 2022: 9 · 2021: 14 · 2020: 12 · 2019: 8 · 2018: 8 · 2017: 4 · 2016: 6 · 2015: 4 · 2014: 11 · 2013: 9 · 2012: 9
- FWCI
- 1.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biology of Reproduction (publishedVersion)
- PubMed (publishedVersion)
- BioOne Complete (BioOne) (submittedVersion)
- Funders
- National Institutes of Health (1r15hd037950-01a1, 5r03hd037672-02)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-37672, HD-37950)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Health Sciences › Medicine › Reproductive Medicine › Reproductive Biology and Fertility
- Keywords
- growth hormone, insulin-like growth factor I, somatotropic axis, puberty onset, fertility, folliculogenesis, ovulation, spermatogenesis, Leydig cell function, pituitary gonadotropin secretion, growth hormone receptor knockout mice, Laron syndrome, GH resistance, dwarfism, corpus luteum, gonadal function
- MeSH terms
- Animals, Humans, Insulin-Like Growth Factor I, Reproduction, Growth Hormone
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