Emerging Roles of Anti-Müllerian Hormone in Hypothalamic-Pituitary Function

Barbotin, Anne‐Laure; Peigné, Maëliss; Malone, Samuel A.; Giacobini, Paolo

doi:10.1159/000500689

Cited by 51 publications

(45 citation statements)

References 123 publications

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“…Most notably, women with endometriosis exhibit, relative to controls: (1) shorter AGDs, indicative of lower prenatal testosterone [ 40 , 41 ], (2) lower LH relative to FSH, (3) higher SHBG, (4) higher serum oxytocin, (5) lower ovarian and serum testosterone, (6) lower AMH, (7) lower WHR and BMI, (8) lower β-endorphin and (9) a suite of other differences, all of which are opposite to the differences found between PCOS versus controls [ 3 ]. The patterns of differences between women with PCOS and endometriosis are highly concordant with one another: for example, in women without PCOS or endometriosis, higher postnatal serum testosterone has been associated with lower SHBG, longer AGD, higher LH, lower FSH, higher β-endorphin and higher WHR (e.g., [ 3 , 42 , 43 ]).…”

Section: Ontogenymentioning

confidence: 84%

The evolutionary biology of endometriosis

Dinsdale

Nepomnaschy

Crespi

2021

Evolution, Medicine, and Public Health

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We provide the first analysis and synthesis of the evolutionary and mechanistic bases for risk of endometriosis in humans, structured around Niko Tinbergen's four questions about phenotypes: phylogenetic history, development, mechanism, and adaptive significance. Endometriosis, which is characterized by the proliferation of endometrial tissue outside of the uterus, has its phylogenetic roots in the evolution of three causally-linked traits: (1) highly-invasive placentation, (2) spontaneous rather than implantation-driven endometrial decidualization, and (3) frequent extensive estrogen-driven endometrial proliferation and inflammation, followed by heavy menstrual bleeding. Endometriosis is potentiated by these traits, and appears to be driven, proximately, by relatively low levels of prenatal and postnatal testosterone. Testosterone affects the developing HPO (hypothalamic-pituitary-ovarian) axis and at low levels it can result in an altered trajectory of reproductive and physiological phenotypes that in extreme cases can mediate the symptoms of endometriosis. Polycystic ovary syndrome, by contrast, is known from previous work to be caused primarily by high prenatal and postnatal testosterone, and it demonstrates a set of phenotypes opposite to those found in endometriosis. The hypothesis that endometriosis risk is driven by low prenatal testosterone, and involves extreme expression of some reproductive phenotypes, is supported by a suite of evidence from genetics, development, endocrinology, morphology and life history. The hypothesis also provides insights into why these two diametric, fitness-reducing disorders are maintained at such high frequencies in human populations. Finally, the hypotheses described and evaluated here lead to numerous testable predictions, and have direct implications for the treatment and study of endometriosis.

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Section: Ontogenymentioning

confidence: 84%

The evolutionary biology of endometriosis

Dinsdale

Nepomnaschy

Crespi

2021

Evolution, Medicine, and Public Health

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“…The physiological role of AMH and its receptor in post-natal life and, particularly, from birth to puberty, is currently unknown. The presence of AMHR2 outside the gonads, and, particularly, in gonadotropic cells of the anterior pituitary gland and the hypothalamus, suggests a role for AMH as a neuroendocrine regulation of the hypothalamic-pituitary-gonadal function [ 25 ]. Interestingly, clinical evidence indicates that AMH serum levels may help in differentiating the patients with HH from those with delayed puberty in childhood [ 26 , 27 , 28 ].…”

Section: Discussionmentioning

confidence: 99%

Anti-Müllerian Hormone, Growth Hormone, and Insulin-Like Growth Factor 1 Modulate the Migratory and Secretory Patterns of GnRH Neurons

Cannarella

Paganoni

Cicolari

et al. 2021

IJMS

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Anti-Müllerian hormone (AMH) is secreted by Sertoli or granulosa cells. Recent evidence suggests that AMH may play a role in the pathogenesis of hypogonadotropic hypogonadism (HH) and that its serum levels could help to discriminate HH from delayed puberty. Moreover, the growth hormone (GH)/insulin-like growth factor 1 (IGF1) system may be involved in the function of gonadotropin-releasing hormone (GnRH) neurons, as delayed puberty is commonly found in patients with GH deficiency (GHD) or with Laron syndrome, a genetic form of GH resistance. The comprehension of the stimuli enhancing the migration and secretory activity of GnRH neurons might shed light on the causes of delay of puberty or HH. With these premises, we aimed to better clarify the role of the AMH, GH, and IGF1 on GnRH neuron migration and GnRH secretion, by taking advantage of previously established models of immature (GN11 cell line) and mature (GT1-7 cell line) GnRH neurons. Expression of Amhr, Ghr, and Igf1r genes was confirmed in both cell lines. Cells were then incubated with increasing concentrations of AMH (1.5–150 ng/mL), GH (3–1000 ng/mL), or IGF1 (1.5–150 ng/mL). All hormones were able to support GN11 cell chemomigration. AMH, GH, and IGF1 significantly stimulated GnRH secretion by GT1-7 cells after a 90-min incubation. To the best of our knowledge, this is the first study investigating the direct effects of GH and IGF1 in GnRH neuron migration and of GH in the GnRH secreting pattern. Taken together with previous basic and clinical studies, these findings may provide explanatory mechanisms for data, suggesting that AMH and the GH-IGF1 system play a role in HH or the onset of puberty.

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“…The combination of several in vitro and in vivo experiments showed that AMH increased the pulsatile secretion of GnRH-dependent LH through a central action. Indeed, electrophysiological experiments have revealed that exogenous AMH increased the neuronal activity of GnRH neurons; however, this could be an indirect action, as AMHR2 is very widely expressed in the hypothalamic regions, so a synergistic action of other cell types contributing to the increase in GnRH secretion cannot be excluded [for review see ( 59 )]. Similarly, the authors demonstrated that in vivo administration of AMH (intracerebroventricularly) was accompanied by a dose-dependent increase in LH secretion and pulsatility.…”

Section: Role Of Amh In the Gonadotropin Dysregulation Of Pcosmentioning

confidence: 99%

Role of Anti-Müllerian Hormone in the Pathogenesis of Polycystic Ovary Syndrome

et al. 2020

Self Cite

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Besides its interest for diagnosis, the finding of an elevated serum AMH level in PCOS has open major pathophysiological issues. This review addresses the three most important issues: 1-the role of AMH in the disturbed folliculogenesis of PCOS; 2-the role of AMH in the gonadotropin dysregulation of PCOS and 3-the role of AMH in the trans-generational transmission of PCOS. For each of those issues, the clinical and experimental evidences currently available are discussed and pathophysiological hypothesis are proposed.

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Emerging Roles of Anti-Müllerian Hormone in Hypothalamic-Pituitary Function

Cited by 51 publications

References 123 publications

The evolutionary biology of endometriosis

The evolutionary biology of endometriosis

Anti-Müllerian Hormone, Growth Hormone, and Insulin-Like Growth Factor 1 Modulate the Migratory and Secretory Patterns of GnRH Neurons

Role of Anti-Müllerian Hormone in the Pathogenesis of Polycystic Ovary Syndrome

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