Anti-Müllerian hormone - wikipedia Anti-Müllerian hormone anti-Müllerian hormone Identifiers Symbol AMH Entrez 268 HUGO 464 OMIM 600957 RefSeq NM_000479 UniProt P03971 Other data Locus Chr. 19 p13. 3 anti-Müllerian hormone receptor, type II Identifiers Symbol AMHR2 Entrez 269 HUGO 465 OMIM 600956 RefSeq NM_020547 UniProt Q16671 Other data Locus Chr. 12 q13 Anti-Müllerian hormone ( AMH ), also known as Müllerian - inhibiting hormone ( MIH ), is a glycoprotein hormone structurally related to inhibin and activin from the transforming growth factor beta superfamily, whose key roles are in growth differentiation and folliculogenesis. In humans, the gene for AMH is AMH, on chromosome 19p 13.3, while the gene AMHR2 codes for its receptor on chromosome 12. AMH is activated by SOX9 in the Sertoli cells of the male fetus. Its expression inhibits the development of the female reproductive tract, or Müllerian ducts ( paramesonephric ducts ), in the male embryo, thereby arresting the development of fallopian tubes, uterus, and upper vagina. AMH expression is critical to sex differentiation at a specific time during fetal development, and appears to be tightly regulated by nuclear receptor SF - 1, transcription GATA factors, sex - reversal gene DAX1, and follicle - stimulating hormone ( FSH ). Mutations in both the AMH gene and the type II AMH receptor have been shown to cause the persistence of Müllerian derivatives in males that are otherwise normally masculinized. AMH is also a product of granulosa cells of the preantral and small antral follicles in women. As such, AMH is only present in the ovary until menopause. Production of AMH regulates folliculogenesis by inhibiting recruitment of follicles from the resting pool in order to select for the dominant follicle, after which the production of AMH diminishes. As a product of the granulosa cells, which envelop each egg and provide them energy, AMH can also serve as a molecular biomarker for relative size of the ovarian reserve. In humans, this is helpful because the number of cells in the follicular reserve can be used to predict timing of menopause. In bovine, AMH can be used for selection of females in multi-ovulatory embryo transfer programs by predicting the number of antral follicles developed to ovulation. AMH can also be used as a marker for ovarian dysfunction, such as in women with polycystic ovary syndrome ( PCOS ). Contents 1 Structure 2 Function 2.1 Embryogenesis 2.2 Ovarian 2.3 Other 3 Pathology 4 Blood levels 4.1 Reference ranges 5 Clinical usage 5.1 General fertility assessment 5.2 In vitro fertilization 5.3 Natural remedies 5.4 Women with cancer 5.5 Neutering status in animals 5.6 Biomarker of polycystic ovary syndrome 5.7 Potential future usage 6 Names 7 See also 8 References Structure AMH is a dimeric glycoprotein with a molar mass of 140 kDa. The molecule consists of two identical subunits linked by sulfide bridges, and characterized by the N - terminal dimer ( pro-region ) and C - terminal dimer. AMH acts with receptors, AMH - RI and AMH - RII, upon which, after a series of conformational changes and phosphorylation steps, gene expression is regulated in the cell. Function Embryogenesis In mammals, AMH prevents the development of the Müllerian ducts into the uterus and other Müllerian structures. The effect is ipsilateral, that is each testis suppresses Müllerian development only on its own side. In humans, this action takes place during the first 8 weeks of gestation. If no hormone is produced from the gonads, the Müllerian ducts automatically develop, while the Wolffian ducts, which are responsible for male reproductive parts, automatically die. Amounts of AMH that are measurable in the blood vary by age and sex. AMH works by interacting with specific receptors on the surfaces of the cells of target tissues ( anti-Müllerian hormone receptors ). The best - known and most specific effect, mediated through the AMH type II receptors, includes programmed cell death ( apoptosis ) of the target tissue ( the fetal Müllerian ducts ). Ovarian AMH is expressed by granulosa cells of the ovary during the reproductive years, and limits the formation of primary follicles by inhibiting excessive follicular recruitment by FSH. AMH expression is greatest in the recruitment stage of folliculogenesis, in the preantral and small antral follicles. This expression diminishes as follicles develop and enter selection stage, upon which FSH expression increases. Some authorities suggest it is a measure of certain aspects of ovarian function, useful in assessing conditions such as polycystic ovary syndrome and premature ovarian failure. Other AMH production by the Sertoli cells of the testes remains high throughout childhood in males but declines to low levels during puberty and adult life. AMH has been shown to regulate production of sex hormones, and changing AMH levels ( rising in females, falling in males ) may be involved in the onset of puberty in both sexes. Functional AMH receptors have also been found to be expressed in neurons in the brains of embryonic mice, and are thought to play a role in sexually dimorphic brain development and consequent development of gender - specific behaviours. Pathology In men, inadequate embryonal AMH activity can lead to the Persistent Müllerian duct syndrome ( PMDS ), in which a rudimentary uterus is present and testes are usually undescended. The AMH gene ( AMH ) or the gene for its receptor ( AMH - RII ) are usually abnormal. AMH measurements have also become widely used in the evaluation of testicular presence and function in infants with intersex conditions, ambiguous genitalia, and cryptorchidism. A study published in Nature Medicine found a link between hormonal imbalance in the womb and Polycystic ovary syndrome ( PCOS ), specifically prenatal exposure to anti-Müllerian hormone. For the study, the researchers injected pregnant mice with AMH so that they had a higher than normal concentration of the hormone. Indeed, they gave birth to daughters who later developed PCOS - like tendencies. These included problems with fertility, delayed puberty, and erratic ovulation. To reverse it, the researchers dosed the polycystic mice with an IVF drug called cetrorelix, which made the symptoms to go away. These experiments should be confirmed in humans, but it could be the first step in understanding the relationship between the polycystic ovary and the anti-Müllerian hormone. Blood levels In healthy females AMH is either just detectable or undetectable in cord blood at birth and demonstrates a marked rise by three months of age ; while still detectable it falls until four years of age before rising linearly until eight years of age remaining fairly constant from mid-childhood to early adulthood -- it does not change significantly during puberty. The rise during childhood and adolescence is likely reflective of different stages of follicle development. From 25 years of age AMH declines to undetectable levels at menopause. The standard measurement of AMH follows the Generation II assay. This should give the same values as the previously used IBC assay, but AMH values from the previously used DSL assay should be multiplied with 1.39 to conform to current standards because it used different antibodies. Weak evidence suggests that AMH should be measured only in the early follicular phase because of variation over the menstrual cycle. Also, AMH levels decrease under current use of oral contraceptives and current tobacco smoking. Reference ranges Reference ranges for Anti-Müllerian hormone, as estimated from reference groups in the United states, are as follows : Females : Age Unit Value Younger than 24 months ng / mL Less than 5 pmol / l Less than 35 24 months to 12 years ng / mL Less than 10 pmol / l Less than 70 13 -- 45 years ng / mL 1 to 10 pmol / l 7 to 70 More than 45 years ng / mL Less than 1 pmol / l Less than 7 Males : Age Unit Value Younger than 24 months ng / mL 15 to 500 pmol / l 100 to 3500 24 months to 12 years ng / mL 7 to 240 pmol / l 50 to 1700 More than 12 years ng / mL 0.7 to 20 pmol / l 5 to 140 AMH measurements may be less accurate if the person being measured is vitamin D deficient. Note that males are born with higher AMH levels than females in order to initiate sexual differentiation, and in women, AMH levels decrease over time as fertility decreases as well. Clinical usage General fertility assessment Comparison of an individual 's AMH level with respect to average levels is useful in fertility assessment, as it provides a guide to ovarian reserve and identifies women that may need to consider either egg freezing or trying for a pregnancy sooner rather than later if their long - term future fertility is poor. A higher level of anti-Müllerian hormone when tested in women in the general population has been found to have a positive correlation with natural fertility in women aged 30 -- 44 aiming to conceive spontaneously, even after adjusting for age. However, this correlation was not found in a comparable study of younger women ( aged 20 to 35 years ). In vitro fertilization AMH is a predictor for ovarian response in in vitro fertilization ( IVF ). Measurement of AMH supports clinical decisions, but alone it is not a suitable predictor of IVF success. Additionally, AMH levels are used to estimate a woman 's remaining egg supply. According to NICE guidelines of in vitro fertilization, an anti-Müllerian hormone level of less than or equal to 5.4 pmol / l ( 0.8 ng / mL ) predicts a low response to ovarian hyperstimulation, while a level greater than or equal to 25.0 pmol / l ( 3.6 ng / mL ) predicts a high response. Other cut - off values found in the literature vary between 0.7 and 20 pmol / l ( 0.1 and 2.97 ng / ml ) for low response to ovarian hyperstimulation. Subsequently, higher AMH levels are associated with greater chance of live birth after IVF, even after adjusting for age. AMH can thereby be used to rationalise the programme of ovulation induction and decisions about the number of embryos to transfer in assisted reproduction techniques to maximise pregnancy success rates whilst minimising the risk of ovarian hyperstimulation syndrome ( OHSS ). AMH can predict an excessive response in ovarian hyperstimulation with a sensitivity and specificity of 82 % and 76 %, respectively. Measuring AMH alone may be misleading as high levels occur in conditions like polycystic ovarian syndrome and therefore AMH levels should be considered in conjunction with a transvaginal scan of the ovaries to assess antral follicle count and ovarian volume. Natural remedies Studies into treatments to improve low ovarian reserve and low AMH levels have met with some success. Current best available evidence suggests that DHEA improves ovarian function, increases pregnancy chances and, by reducing aneuploidy, lowers miscarriage rates. The studies into DHEA for low AMH show that a dose of 75 mg for a period of 16 weeks should be taken. Improvement of oocyte / embryo quality with DHEA supplementation potentially suggests a new concept of ovarian aging, where ovarian environments, but not oocytes themselves, age. DHEA has positive outcomes for women with AMH levels over 0.8 ng / ml or 5.7 pmol / l DHEA has no apparent effect on oocytes or ovarian environments under this range. Studies on CoQ10 supplementation in an aged animal model delayed depletion of ovarian reserve, restored oocyte mitochondrial gene expression, and improved mitochondrial activity. Authors note that to replicate the 12 -- 16 weeks of using CoQ10 supplements on mice to achieve these results would be the equivalent to a decade in humans. Vitamin D is believed to play a role in AMH regulation. The AMH gene promoter contains a vitamin D response element that may cause vitamin D status to influence serum AMH levels. Women with levels of Vitamin D of 267.8 ± 66.4 nmol / L show a 4 times better success rate with IVF procedure than those with low levels of 104.3 ± 21 nmol / L. Vitamin D deficiency should be considered when serum AMH levels are obtained for diagnosis. Ovance, a Chinese herbal medicine formula has shown success at treating low AMH levels and improving pregnancy outcomes. Studies report increases in serum AMH levels in women with 0.0028 ng / ml or 0.02 pmol / l. Pregnancy was very low at AMH ≤ 0.04 ng / mL but significantly increased at AMH 0.41 -- 1.05 ng / mL, resulting in similarly low live - birth rates at all AMH levels ≤ 1.05 ng / mL and significantly improved live - birth rates at AMH ≥ 1.06 ng / mL. Women with cancer In women with cancer, radiation therapy and chemotherapy can damage the ovarian reserve. In such cases, a pre-treatment AMH is useful in predicting the long - term post-chemotherapy loss of ovarian function, which may indicate fertility preservation strategies such as oocyte cryopreservation. A post-treatment AMH is associated with decreased fertility. Granulosa cell tumors of the ovary secrete AMH, and AMH testing has a sensitivity ranging between 76 and 93 % in diagnosing such tumors. AMH is also useful in diagnosing recurrence of granulosa cell tumors. Neutering status in animals In veterinary medicine, AMH measurements are used to determine neutering status in male and female dogs and cats. AMH levels can also be used to diagnose cases of ovarian remnant syndrome. Biomarker of polycystic ovary syndrome Polycystic ovary syndrome ( PCOS ) is an endocrine disorder most commonly found in women of reproductive age that is characterized by oligo - or anovulation, hyperandrogenism, and polycystic ovaries ( PCO ). This endocrine disorder increases AMH levels at nearly two to three times higher in women with PCOS than in normal type women. This is often attributed to the increased follicle count number characteristic of PCOS, indicating an increase in granulosa cells since they surround each individual egg. However, increased AMH levels have also been attributed not just to the increased number of follicles, but also to an increased amount of AMH produced per follicle. The high levels of androgens, characteristic of PCOS, also stimulate and provide feedback for increased production of AMH, as well. In this way, AMH has been increasingly considered to be a tool or biomarker that can be used to diagnose or indicate PCOS. Potential future usage AMH has been synthesized. Its ability to inhibit growth of tissue derived from the Müllerian ducts has raised hopes of usefulness in the treatment of a variety of medical conditions including endometriosis, adenomyosis, and uterine cancer. Research is underway in several laboratories. If there were more standardized AMH assays, it could potentially be used as a biomarker of polycystic ovary syndrome. In mice, an increase in AMH has been shown to reduce the number of growing follicles and thus the overall size of the ovaries. This increase in AMH production reduces primary, secondary and antral follicles without reducing the number of primordial follicles suggesting a blockade of primordial follicle activation. This may provide a viable method of contraception which protects the ovarian reserve of oocytes during chemotherapy without extracting them from the body allowing the potential for natural reproduction later in life. Names The adjective `` Müllerian '' is written either `` Müllerian '' or `` müllerian '', depending on the governing style guide ; the derived term with the prefix of `` anti - '' is then `` anti-Müllerian '', `` anti-müllerian '', or `` antimüllerian ''. The Müllerian ducts are named after Johannes Peter Müller. A list of the names that have been used for the antimüllerian hormone is as follows. For the sake of simplicity, this list ignores some orthographic variations ; for example, it gives only one row for `` Müllerian - inhibiting hormone '', although there are 4 acceptable stylings thereof ( cap M or lowercase m, hyphen or space ). Protein name styling Protein symbol Anti-Müllerian hormone AMH Müllerian - inhibiting factor MIF Müllerian - inhibiting hormone MIH Müllerian - inhibiting substance MIS Müllerian duct inhibitory factor MDIF Müllerian regression factor MRF Anti-paramesonephric hormone APH See also Sexual differentiation Anti-Müllerian hormone receptor Alfred Jost discoverer. PMDS ( Persistent Müllerian Duct Syndrome ) References ^ Jump up to : Rzeszowska M, Leszcz A, Putowski L, Hałabiś M, Tkaczuk - Włach J, Kotarski J, Polak G ( 2016 ). `` Anti-Müllerian hormone : structure, properties and appliance ''. Ginekologia Polska. 87 ( 9 ) : 669 -- 674. doi : 10.5603 / gp. 2016.0064. PMID 27723076. Jump up ^ Cate RL, Mattaliano RJ, Hession C, Tizard R, Farber NM, Cheung A, Ninfa EG, Frey AZ, Gash DJ, Chow EP ( June 1986 ). `` Isolation of the bovine and human genes for Müllerian inhibiting substance and expression of the human gene in animal cells ''. 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Jump up ^ Dewailly D, Lujan ME, Carmina E, Cedars MI, Laven J, Norman RJ, Escobar - Morreale HF ( 2013 ). `` Definition and significance of polycystic ovarian morphology : a task force report from the Androgen Excess and Polycystic Ovary Syndrome Society ''. Human Reproduction Update. 20 ( 3 ) : 334 -- 52. doi : 10.1093 / humupd / dmt061. PMID 24345633. Jump up ^ Kano M, Sosulski AE, Zhang L, Saatcioglu HD, Wang D, Nagykery N, Sabatini ME, Gao G, Donahoe PK, Pépin D ( February 2017 ). `` AMH / MIS as a contraceptive that protects the ovarian reserve during chemotherapy ''. Proceedings of the National Academy of Sciences of the United States of America. 114 ( 9 ) : E1688 -- E1697. doi : 10.1073 / pnas. 1620729114. PMC 5338508. PMID 28137855. Jump up ^ Minkoff E, Baker P ( 2004 ). Biology Today : An Issues Approach ( Third ed. ). New York : Garland Science. p. 296. ISBN 978 - 1 - 136 - 83875 - 0. Hormones Endocrine glands Hypothalamic - pituitary Hypothalamus GnRH TRH Dopamine CRH GHRH Somatostatin ( GHIH ) MCH Posterior pituitary Oxytocin Vasopressin Anterior pituitary FSH LH TSH Prolactin POMC CLIP ACTH MSH Endorphins Lipotropin GH Adrenal axis Adrenal cortex aldosterone cortisol cortisone DHEA DHEA - S androstenedione Adrenal medulla epinephrine norepinephrine Thyroid Thyroid hormones Calcitonin Thyroid axis Parathyroid PTH Gonadal axis Testis testosterone AMH inhibin Ovary estradiol progesterone activin and inhibin relaxin Placenta hCG HPL estrogen progesterone Pancreas glucagon insulin amylin somatostatin pancreatic polypeptide Pineal gland melatonin N, N - dimethyltryptamine 5 - methoxy - N, N - dimethyltryptamine Other Thymus Thymosins Thymosin α1 Beta thymosins Thymopoietin Thymulin Digestive system Stomach gastrin ghrelin Duodenum CCK Incretins GIP GLP - 1 secretin motilin VIP Ileum enteroglucagon peptide YY Liver / other Insulin - like growth factor IGF - 1 IGF - 2 Adipose tissue leptin adiponectin resistin Skeleton Osteocalcin Kidney renin EPO calcitriol prostaglandin Heart Natriuretic peptide ANP BNP Cell signaling : TGFβ signaling pathway TGF beta superfamily of ligands TGF beta family TGF - β1 TGF - β2 TGF - β3 Bone morphogenetic proteins BMP2 BMP3 BMP4 BMP5 BMP6 BMP7 BMP8a BMP8b BMP10 BMP15 Growth differentiation factors GDF1 GDF2 GDF3 GDF5 GDF6 GDF7 Myostatin / GDF8 GDF9 GDF10 GDF11 GDF15 Other Activin and inhibin Anti-müllerian hormone Nodal TGF beta receptors ( Activin, BMP ) TGFBR1 : Activin type 1 receptors ACVR1 ACVR1B ACVR1C ACVRL1 BMPR1 BMPR1A BMPR1B TGFBR2 : Activin type 2 receptors ACVR2A ACVR2B AMHR2 BMPR2 TGFBR3 : betaglycan Transducers / SMAD R - SMAD ( SMAD1 SMAD2 SMAD3 SMAD5 SMAD9 ) I - SMAD ( SMAD6 SMAD7 ) SMAD4 Ligand inhibitors Cerberus Chordin Decorin Follistatin Gremlin Lefty LTBP1 Noggin PARN THBS1 Coreceptors BAMBI Cripto Other SARA TGFβ receptor superfamily modulators Type I ALK1 ( ACVRL1 ) Agonists : Activin ( A, B, AB ) Avotermin BMP ( 10 ) Cetermin GDF ( 2 ( BMP9 ) ) TGFβ ( 1, 2, 3 ) Antibodies : Ascrinvacumab Kinase inhibitors : K - 02288 ML - 347 ( LDN - 193719, VU0469381 ) Decoy receptors : Dalantercept Other inhibitors : Disitertide ALK2 ( ACVR1A ) Agonists : Activin ( A, B, AB ) AMH ( MIS ) Avotermin BMP ( 5, 6, 7, 8A, 8B ) Eptotermin alfa TGFβ ( 1, 2, 3 ) Kinase inhibitors : DMH - 1 DMH - 2 Dorsomorphin ( BML - 275 ) K - 02288 ML - 347 ( LDN - 193719, VU0469381 ) ALK3 ( BMPR1A ) Agonists : AMH ( MIS ) BMP ( 2, 4, 5, 6, 7, 8A, 8B ) Dibotermin alfa Eptotermin alfa Kinase inhibitors : DMH - 2 Dorsomorphin ( BML - 275 ) K - 02288 ALK4 ( ACVR1B ) Agonists : Activin ( A, B, AB ) GDF ( 1, 3, 11 ( BMP11 ) ) Myostatin ( GDF8 ) Nodal Antagonists : Inhibin ( A, B) Lefty ( 1, 2 ) Kinase inhibitors : A 83 - 01 SB - 431542 SB - 505124 ALK5 ( TGFβR1 ) Agonists : Avotermin GDF ( 10 ( BMP3B ), 11 ( BMP11 ) ) TGFβ ( 1, 2, 3 ) Antibodies : Fresolimumab Lerdelimumab Metelimumab Kinase inhibitors : A 83 - 01 D - 4476 GW - 788388 LY - 364947 LY - 2109761 Galunisertib ( LY - 2157299 ) R - 268712 RepSox ( E-616452, SJN - 2511 ) SB - 431542 SB - 505124 SB - 525334 SD - 208 ALK6 ( BMPR1B ) Agonists : BMP ( 2, 4, 5, 6, 7, 8A, 8B, 15 ( GDF9B ) ) Dibotermin alfa Eptotermin alfa GDF ( 5 ( BMP14 ), 6 ( BMP13 ), 7 ( BMP12 ), 9, 15 ) Radotermin Kinase inhibitors : DMH - 2 Dorsomorphin ( BML - 275 ) K - 02288 ALK7 ( ACVR1C ) Agonists : GDF ( 1, 3, 11 ( BMP11 ) ) Nodal Antagonists : Lefty ( 1, 2 ) Kinase inhibitors : A 83 - 01 SB - 431542 SB - 505124 Type II TGFβR2 Agonists : Avotermin GDF ( 10 ( BMP3B ) ) TGFβ ( 1, 2, 3 ) Antibodies : Fresolimumab Lerdelimumab Metelimumab Kinase inhibitors : DMH - 2 LY - 364947 BMPR2 Agonists : BMP ( 2, 4, 6, 7, 10 ) Dibotermin alfa Eptotermin alfa GDF ( 2 ( BMP9 ), 5 ( BMP14 ), 6 ( BMP13 ), 7 ( BMP12 ) ) Radotermin Antagonists : Inhibin ( A, B) ACVR2A ( ACVR2 ) Agonists : Activin ( A, B, AB ) BMP ( 2, 4, 5, 6, 7, 8A, 8B, 15 ( GDF9B ) ) Dibotermin alfa Eptotermin alfa GDF ( 1, 3, 5 ( BMP14 ), 6 ( BMP13 ), 7 ( BMP12 ), 9, 11 ( BMP11 ), 15 ) Myostatin ( GDF8 ) Nodal Radotermin Antagonists : Inhibin ( A, B) Lefty ( 1, 2 ) Decoy receptors : Sotatercept ACVR2B Agonists : Activin ( A, B, AB ) BMP ( 2, 4, 6, 7 ) Dibotermin alfa Eptotermin alfa GDF ( 1, 3, 5 ( BMP14 ), 6 ( BMP13 ), 7 ( BMP12 ) ) Myostatin ( GDF8 ) Nodal Osteogenin ( BMP3, BMP3A ) Radotermin Antagonists : Inhibin ( A, B) Lefty ( 1, 2 ) Decoy receptors : Ramatercept AMHR2 ( AMHR ) Agonists : AMH ( MIS ) Type III TGFβR3 ( β - glycan ) Ligands : Avotermin Inhibin ( A, B) TGFβ ( 1, 2, 3 ) Unsorted Endogenous antagonists / inhibitors : BAMBI Cerberus ( CER1 ) Chordin DAN ( PARN ) Decorin Follistatin Gremlin ( Drm ) LTBP1 Noggin TGIF Thrombospondin 1 ( THBS1 ) Tomoregulin 1 Antibodies : Stamulumab ( against myostatin ) TRC105 ( against endoglin ) Others : Endoglin See also Receptor / signaling modulators Signaling peptide / protein receptor modulators Growth factor receptor modulators Cytokine receptor modulators Retrieved from `` https://en.wikipedia.org/w/index.php?title=Anti - Müllerian_hormone&oldid = 841477221 '' Categories : Genes on human chromosome 19 Genes on human chromosome 12 Animal developmental biology Fish hormones Hormones of the embryo Hidden categories : Protein pages needing a picture Use dmy dates from April 2017 Talk Contents About Wikipedia Deutsch Español Français Galego Italiano עברית Nederlands Polski Português Русский Српски / srpski Srpskohrvatski / српскохрватски Svenska Türkçe 中文 6 more Edit links This page was last edited on 16 May 2018, at 02 : 59. 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Question: when the testis does not produce anti-müllerian hormone the müllerian ducts develop into
Answer: the development of the female reproductive tract