Pituitary Control of Ovarian Function — Concepts Derived from Gonadotrophin Therapy

Brown, J. B.

doi:10.1111/j.1479-828x.1978.tb00011.x

Cited by 297 publications

(135 citation statements)

References 13 publications

Supporting

Mentioning

124

Contrasting

Unclassified

Order By: Relevance

“…This study, also, suggested that both polymorphisms contribute to the individual variation in the FSH "threshold" [18]. This concept was initially introduced by Brown [19] and now constitutes the basis for gonadotropin administration in controlled ovarian stimulation (COS) in order to achieve multiple follicular growth [20,21]. The maintenance of follicles' growth in order to reach the pre-ovulatory stage depends on whether FSH levels surpass a distinct concentration (FSH "threshold") or not.…”

mentioning

confidence: 97%

See 1 more Smart Citation

Single nucleotide polymorphisms in the Anti-Müllerian hormone (AMH Ile49Ser) and Anti-Müllerian hormone type II receptor (AMHRII −482 A>G) as genetic markers in assisted reproduction technology

Karagiorga

Partsinevelos

Mavrogianni

et al. 2014

J Assist Reprod Genet

View full text Add to dashboard Cite

Purpose The aim of the study was to evaluate whether the presence Antimullerian hormone (AMH) and Antimullerian hormone type II receptor (AMHRII) single nucleotide polymorphisms (SNPs) Ile 49 Ser and -482A>G respectively are related to the assisted reproduction outcome. Methods A prospective cross-sectional observational study was conducted in order to assess the distribution of AMH and AMHRII SNPs in two cohorts, one of healthy women (N=100) and the control group and the IVF/ICSI group (N=151) consisted of women undergoing IVF/ICSI treatment for infertility. Furthermore, a prospective longitudinal observational study was performed on the latter group to assess possible associations of these SNPs with patients' characteristics and controlled ovarian stimulation (COS) and pregnancy outcome. Results Among non-carriers of the AMH (Ile 49 Ser) polymorphism, basal FSH levels were lower in those with more than two of previous IVF attempts and fertilization rate was statistically higher in those with peak serum E2 levels below 1500 pg/ml, whereas among non-carriers of the AMHRII (−482 A>G) polymorphism, number of follicles was higher in those with more than two previous IVF attempts and total dose of gonadotropins was lower in those with peak serum E2 levels above 1500 pg/ml. Conclusions There was evidence that in specific subgroups of women undergoing IVF/ICSI, AMH and AMHRII SNPs may be related to patients' characteristics and controlled ovarian stimulation and pregnancy outcome and thus may provide a means for the prediction of ovarian response in specific subgroups of women entering an IVF/ICSI program.

show abstract

mentioning

confidence: 97%

“…In women, AMH is produced exclusively in the ovary by the granulosa cells of pre-antral and small antral follicles. The gene for AMH is located on chromosome 19 and consists of 5 exons [9,10]. The expression pattern of AMH seems to be similar in mice and human ovary.…”

mentioning

confidence: 99%

Single nucleotide polymorphisms in the Anti-Müllerian hormone (AMH Ile49Ser) and Anti-Müllerian hormone type II receptor (AMHRII −482 A>G) as genetic markers in assisted reproduction technology

Karagiorga

Partsinevelos

Mavrogianni

et al. 2014

J Assist Reprod Genet

View full text Add to dashboard Cite

show abstract

“…During the menstrual cycle, preantral follicles that encompass developing oocytes mature to a preovulatory stage in response to elevated levels of FSH (4). Administration of exogenous FSH also restores follicle development in anovulatory women (5). Finally, mice harboring null alleles for either the FSH receptor or FSH␤ lack preovulatory follicles and are infertile (6,7).…”

mentioning

confidence: 99%

Insulin Receptor Substrate 1, the Hub Linking Follicle-stimulating Hormone to Phosphatidylinositol 3-Kinase Activation

Law

Hunzicker-Dunn

2016

Journal of Biological Chemistry

View full text Add to dashboard Cite

The ubiquitous phosphatidylinositol 3-kinase (PI3K) signaling pathway regulates many cellular functions. However, the mechanism by which G protein-coupled receptors (GPCRs) signal to activate PI3K is poorly understood. We have used ovarian granulosa cells as a model to investigate this pathway, based on evidence that the GPCR agonist follicle-stimulating hormone (FSH) promotes the protein kinase A (PKA)-dependent phosphorylation of insulin receptor substrate 1 (IRS1) on tyrosine residues that activate PI3K. We report that in the absence of FSH, granulosa cells secrete a subthreshold concentration of insulin-like growth factor-1 (IGF-1) that primes the IGF-1 receptor (IGF-1R) but fails to promote tyrosine phosphorylation of IRS1. FSH via PKA acts to sensitize IRS1 to the tyrosine kinase activity of the IGF-1R by activating protein phosphatase 1 (PP1) to promote dephosphorylation of inhibitory Ser/Thr residues on IRS1, including Ser 789 . Knockdown of PP1␤ blocks the ability of FSH to activate PI3K in the presence of endogenous IGF-1. Activation of PI3K thus requires both PKA-mediated relief of IRS1 inhibition and IGF-1R-dependent tyrosine phosphorylation of IRS1. Treatment with FSH and increasing concentrations of exogenous IGF-1 triggers synergistic IRS1 tyrosine phosphorylation at PI3K-activating residues that persists downstream through protein kinase B (AKT) and FOXO1 (forkhead box protein O1) to drive synergistic expression of genes that underlies follicle maturation. Based on the ability of GPCR agonists to synergize with IGFs to enhance gene expression in other cell types, PP1 activation to relieve IRS1 inhibition may be a more general mechanism by which GPCRs act with the IGF-1R to activate PI3K/AKT.The phosphatidylinositol-3 kinase (PI3K) signaling pathway regulates transcription, translation, proliferation, and apoptosis (1, 2). Whereas PI3K is classically activated by receptor tyrosine kinases, such as the insulin-like growth factor-1 receptor (IGF-1R), 2 PI3K is also activated in many cells by G-proteincoupled receptors (GPCRs). However, the mechanisms by which GPCRs signal to activate PI3K are much less understood compared with classical activation by receptor tyrosine kinases (1). We have used rat ovarian granulosa cells (GCs) as a model to elucidate the mechanism by which the GPCR agonist folliclestimulating hormone (FSH) activates PI3K, based on prior evidence that FSH activates PI3K in a protein kinase A (PKA)-dependent manner (3). FSH is an obligatory regulator of ovarian follicle maturation. During the menstrual cycle, preantral follicles that encompass developing oocytes mature to a preovulatory stage in response to elevated levels of FSH (4). Administration of exogenous FSH also restores follicle development in anovulatory women (5). Finally, mice harboring null alleles for either the FSH receptor or FSH␤ lack preovulatory follicles and are infertile (6, 7). Traditionally, FSH has thus been considered both necessary and sufficient to promote follicle maturation.FSH acts exclusively on GCs wit...

show abstract

“…This suggests that there are qualitative differences in the hormones (Wide, 1985) or that the number of follicles ovulating is mediated through influences other than the gonadotrophins. However, the radioimmunoassays (RIAs) used to measure FSH and LH may have been insensitive to the relatively small increases in gonadotrophin concentrations required to cause an increase in ovulation rate (Brown, 1978 (Davis et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

Induction of ovulation in chronically hypophysectomized Booroola ewes

Fry¹,

Clarke

Cummins

et al. 1988

Reproduction

View full text Add to dashboard Cite

Summary. Booroola Merino ewes, with (F+; N = 17) and without (++; N = 13) a copy of the fecundity gene were hypophysectomized and 6 weeks later were given an i.m. injection of PMSG (high, medium or low dose) followed by hCG. The induced ovulation rates were observed laparoscopically. Ovulation rates were significantly higher (P < 0\m=.\01) in Booroola F+ ewes than in ++ ewes (8\m=.\00 \m=+-\1\m=.\66s.e.m. vs 3\m=.\62\m=+-\ 1 \ m= . \ 1 0 respectively). This suggests that the high fecundity of the Booroola ewe may be due primarily to ovarian rather than pituitary factors.

show abstract

Pituitary Control of Ovarian Function — Concepts Derived from Gonadotrophin Therapy

Cited by 297 publications

References 13 publications

Single nucleotide polymorphisms in the Anti-Müllerian hormone (AMH Ile49Ser) and Anti-Müllerian hormone type II receptor (AMHRII −482 A>G) as genetic markers in assisted reproduction technology

Single nucleotide polymorphisms in the Anti-Müllerian hormone (AMH Ile49Ser) and Anti-Müllerian hormone type II receptor (AMHRII −482 A>G) as genetic markers in assisted reproduction technology

Insulin Receptor Substrate 1, the Hub Linking Follicle-stimulating Hormone to Phosphatidylinositol 3-Kinase Activation

Induction of ovulation in chronically hypophysectomized Booroola ewes

Contact Info

Product

Resources

About