AMH/MIS: what we know already about the gene, the protein and its regulation

Rey, Rodolfo; Lukas-Croisier, C.; Lasala, Celina; Bedecarrás, Patricia

doi:10.1016/j.mce.2003.09.007

Cited by 235 publications

(181 citation statements)

References 104 publications

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“…The AMH gene is located on chromosome 19 (Cohen-Haguenauer et al 1987, Cate et al 1990) and encodes a 140 kDa dimeric glycoprotein. AMH is synthesised as a pro-hormone, which undergoes cleavage at the site of action to generate a biologically active C-terminal fragment (Pepinsky et al 1988, Wilson et al 1993, Rey et al 2003.…”

Section: Introductionmentioning

confidence: 99%

Anti-Müllerian hormone and polycystic ovary syndrome: a mountain too high?

Pellatt¹,

Rice²,

Mason³

2010

Reproduction

190

112

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Anti-Mü llerian hormone (AMH) was initially thought to be produced solely by the foetal male during sexual differentiation to promote regression of the Mü llerian ducts. Over the last decade, however, a new and interesting role has emerged for AMH in the ovary. In human ovaries, AMH is produced by granulosa cells from 36 weeks of gestation until menopause, with the highest expression being in small antral follicles. AMH production gradually declines as follicles grow; once follicles reach a size at which they are dominant, it has largely disappeared. Its removal from these larger follicles appears to be an important requirement for dominant follicle selection and progression to ovulation as AMH has an inhibitory role in the ovary, reducing both primordial follicle initiation and follicle sensitivity to FSH by inhibition of aromatase. It is for this reason that AMH is a focus of interest in polycystic ovary syndrome (PCOS). Serum levels are doubled, and granulosa cell production is greatly increased. Interestingly, there appear to be two groups of women with PCOS who can be distinguished by their AMH level: one group consists of those who have high levels which do not reduce with treatment and who respond less well to induction of ovulation, and a second group consists of those in whom the level is less elevated and reduces on treatment and who seem to respond rather better. Understanding the reason for the raised AMH in PCOS may give clues as to the mechanism of anovulation. To conclude, AMH appears to have a major inhibitory role during folliculogenesis, which may contribute to anovulation in PCOS.

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Section: Introductionmentioning

confidence: 99%

Anti-Müllerian hormone and polycystic ovary syndrome: a mountain too high?

Pellatt¹,

Rice²,

Mason³

2010

Reproduction

190

112

View full text Add to dashboard Cite

show abstract

“…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

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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.

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“…While the expression of inhibin B b-subunit is dependent on the coexistence of spermatogenesis (21,22), AMH expression is downregulated by meiotic germ cells (23). In the men, in our study, suppression of spermatogenesis due to the lack of testosterone could stimulate AMH and inhibit inhibin B expression.…”

Section: Discussionmentioning

confidence: 50%

Relationships between FSH, inhibin B, anti-Mullerian hormone, and testosterone during long-term treatment with the GnRH-agonist histrelin in patients with prostate cancer

Eldar‐Geva

Liberty

Chertin

et al. 2010

European Journal of Endocrinology

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Objectives: Medical castration with long-acting GnRH-agonist (GnRHa) is a well-established treatment for metastatic prostate cancer. Our aim was to explore the relationships between FSH, inhibin B, antiMullerian hormone (AMH), and testosterone during treatment with an implant releasing GnRHa. Design: Analysis of hormone levels in frozen serum samples. Methods: Ten patients aged 77G7 (meansGS.E.M.) years with prostate cancer were treated with the GnRHa histrelin for at least a year. Two weeks prior to insertion and for 3-4 months following removal the patients were treated with the antiandrogen flutamide. Serum inhibin B, FSH, testosterone, and AMH levels were measured retrospectively. Results: FSH, inhibin B, and testosterone increased during antiandrogen administration and levels fell after implant insertion. Four weeks post insertion, FSH gradually increased while inhibin B and testosterone remained fully suppressed. AMH levels did not change during antiandrogen treatment, but increased following implant insertion and remained elevated for the duration of implant use. Following removal, FSH and testosterone increased, inhibin B remained low, while AMH decreased. Conclusions: The secondary increase in FSH following initial suppression with the implant is probably related to impaired inhibin B secretion. The lack of inhibin B response to the secondary increase in FSH suggests that long-term exposure of Sertoli-cells to GnRHa impairs their function. This effect appears to be selective since unlike inhibin B, AMH increased. In the absence of testosterone, FSH has a role in AMH regulation.

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AMH/MIS: what we know already about the gene, the protein and its regulation

Cited by 235 publications

References 104 publications

Anti-Müllerian hormone and polycystic ovary syndrome: a mountain too high?

Anti-Müllerian hormone and polycystic ovary syndrome: a mountain too high?

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

Relationships between FSH, inhibin B, anti-Mullerian hormone, and testosterone during long-term treatment with the GnRH-agonist histrelin in patients with prostate cancer

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