Influence of estradiol on insulin-like growth factor-1-induced luteinizing hormone secretion

Hiney, Jill K.; Srivastava, Vinod K.; Dearth, Robert K.; Dees, W. Les

doi:10.1016/j.brainres.2004.03.054

Cited by 24 publications

(35 citation statements)

References 21 publications

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“…Primate studies have shown that IGF-1 treatment decreases the negative feedback effects of estrogen on LH release to advance the onset of puberty (47). Furthermore, the effect of intracerebroventricular IGF-1 treatment on rodent LH release is enhanced if detectable levels of serum estradiol are present (48). These effects are IGF-1R dependent (49).…”

Section: Discussionmentioning

confidence: 87%

Divergent roles of growth factors in the GnRH regulation of puberty in mice

et al. 2010

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Pubertal onset, initiated by pulsatile gonadotropin-releasing hormone (GnRH), only occurs in a favorable, anabolic hormonal milieu. Anabolic factors that may signal nutritional status to the hypothalamus include the growth factors insulin and IGF-1. It is unclear which hypothalamic neuronal subpopulation these factors affect to ultimately regulate GnRH neuron function in puberty and reproduction. We examined the direct role of the GnRH neuron in growth factor regulation of reproduction using the Cre/lox system. Mice with the IR or IGF-1R deleted specifically in GnRH neurons were generated. Male and female mice with the IR deleted in GnRH neurons displayed normal pubertal timing and fertility, but male and female mice with the IGF-1R deleted in GnRH neurons experienced delayed pubertal development with normal fertility. With IGF-1 administration, puberty was advanced in control females, but not in females with the IGF-1R deleted in GnRH neurons, in control males, or in knockout males. These mice exhibited developmental differences in GnRH neuronal morphology but normal number and distribution of neurons. These studies define the role of IGF-1R signaling in the coordination of somatic development with reproductive maturation and provide insight into the mechanisms regulating pubertal timing in anabolic states.

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Section: Discussionmentioning

confidence: 87%

Divergent roles of growth factors in the GnRH regulation of puberty in mice

et al. 2010

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“…Neurotrophic factors may also play a similar role, and I would like to propose the hypothalamic insulin-like growth factor-1 (IGF-1) system as a target for neuroendocrine disruption. My laboratory and others have shown that IGF-1 regulates GnRH release and gene expression, and that this is subject to developmental regulation [74,75,37]. The IGF-1 system is also steroid sensitive [75,48,101].…”

Section: Other Hypothalamic Neurotransmitter and Neurotrophic Factor mentioning

confidence: 96%

“…My laboratory and others have shown that IGF-1 regulates GnRH release and gene expression, and that this is subject to developmental regulation [74,75,37]. The IGF-1 system is also steroid sensitive [75,48,101]. Moreover, GnRH neurons co-express both IGF-1 and IGF-1 receptors [37,38] suggesting the possibility of autocrine regulation of cells co-expressing GnRH and IGF-1 via the IGF-1 receptor.…”

Section: Other Hypothalamic Neurotransmitter and Neurotrophic Factor mentioning

confidence: 99%

Developmental programming and endocrine disruptor effects on reproductive neuroendocrine systems

Gore¹

2008

Frontiers in Neuroendocrinology

230

122

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The ability of a species to reproduce successfully requires the careful orchestration of developmental processes during critical time points, particularly the late embryonic and early postnatal periods. This article begins with a brief presentation of the evidence for how gonadal steroid hormones exert these imprinting effects upon the morphology of sexually differentiated hypothalamic brain regions, the mechanisms underlying these effects, and their implications in adulthood. Then, I review the evidence that aberrant exposure to hormonally-active substances such as exogenous endocrine-disrupting chemicals (EDCs), may result in improper hypothalamic programming, thereby decreasing reproductive success in adulthood. The field of endocrine disruption has shed new light on the discipline of basic reproductive neuroendocrinology through studies on how early life exposures to EDCs may alter gene expression via non-genomic, epigenetic mechanisms, including DNA methylation and histone acetylation. Importantly, these effects may be transmitted to future generations if the germline is affected via transgenerational, epigenetic actions. By understanding the mechanisms by which natural hormones and xenobiotics affect reproductive neuroendocrine systems, we will gain a better understanding of normal developmental processes, as well as to develop the potential ability to intervene when development is disrupted.

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“…In the pituitary, IGF1 stimulates the secretion of luteinizing hormone (30). In the ovary, IGF1 has also been found to be a key regulator of estrogen synthesis through regulation of aromatase expression and activity (31,32).…”

Section: Discussionmentioning

confidence: 99%

Genetic coregulation of age of female sexual maturation and lifespan through circulating IGF1 among inbred mouse strains

Yuan

Meng

Nautiyal

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

103

105

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We previously reported that mouse strains with lower circulating insulin-like growth factor 1 (IGF1) level at 6 mo have significantly extended longevity. Here we report that strains with lower IGF1 have significantly delayed age of female sexual maturation, measured by vaginal patency (VP). Among strains with normal lifespans (mean lifespan >600 d), delayed age of VP associated with greater longevity (P = 0.015), suggesting a genetically regulated tradeoff at least partly mediated by IGF1. Supporting this hypothesis, C57BL/6J females had 9% lower IGF1, 6% delayed age of VP, and 24% extended lifespan compared with C57BL/6J.C3H/HeJ-Igf1, which carries a C3H/HeJ allele on chromosome (Chr) 10 that increases IGF1. To identify genetic loci/genes that regulate female sexual maturation, including loci that mediate lifespan tradeoffs, we performed haplotype association mapping for age of VP and identified significant loci on Chrs 4 (Vpq1) and 16 (Vpq2 and 3). At each locus, wildderived strains share a unique haplotype that associates with delayed VP. Substitution of Chr 16 of C57BL/6J with Chr 16 from a wild-derived strain significantly reduced IGF1 and delayed VP. Strains with a wild-derived allele at Vpq3 have significantly extended longevity compared with strains with other alleles. Bioinformatic analysis identified Nrip1 at Vpq3 as a candidate gene. Nrip1−/− females have significantly reduced IGF1 and delayed age of VP compared with Nrip1 +/+ females. We conclude that IGF1 may coregulate female sexual maturation and longevity; wild-derived strains carry specific alleles that delay sexual maturation; and Nrip1 is involved in regulating sexual maturation and may affect longevity by regulating IGF1 level.aging | reproduction | hormone E pidemiology studies have suggested that sexual maturation is genetically regulated (1, 2). According to evolutionary theory, natural selection plays an important role in selecting alleles that regulate female sexual maturation (3-5). The evolutionary theory of aging predicts that the timing of female sexual maturation is linked to the rate of aging by pleiotropic genes that mediate a tradeoff between sexual maturation and aging (6, 7). This theory is supported by a field population study of mammalian species ranging from mouse to elephant that identified a positive correlation between age of reproduction and lifespan (8). In rodent, caloric restriction delays female maturity and slows aging (9). Also, reduced female reproduction and extended longevity were found in most models that carry mutations in genes of the growth hormone/insulin-like growth factor 1 (IGF1) pathway (10). These studies suggest that the set of genes that regulate sexual maturation includes a subset of pleiotropic genes that mediate a lifehistory tradeoff between development and aging.Previous studies have suggested that considerable genetic variance of female reproductive development exists within Mus musculus. However, before our study, the age of sexual maturation of inbred strains had not been systematically measu...

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Influence of estradiol on insulin-like growth factor-1-induced luteinizing hormone secretion

Cited by 24 publications

References 21 publications

Divergent roles of growth factors in the GnRH regulation of puberty in mice

Divergent roles of growth factors in the GnRH regulation of puberty in mice

Developmental programming and endocrine disruptor effects on reproductive neuroendocrine systems

Genetic coregulation of age of female sexual maturation and lifespan through circulating IGF1 among inbred mouse strains

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