Table of Contents  
REVIEW
Year : 2019  |  Volume : 21  |  Issue : 2  |  Page : 109-114

Regulation of anti-Müllerian hormone (AMH) in males and the associations of serum AMH with the disorders of male fertility


1 Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing 100191, China
2 Key Laboratory of Assisted Reproduction, Ministry of Education, Beijing 100191, China
3 National Clinical Research Center for Obstetrics and Gynecology, Beijing 100191, China
4 Beijing Key Laboratory of Reproductive Endocrinology and Assisted Reproductive Technology, Beijing 100191, China
5 Department of Urology, Peking University Third Hospital, Beijing 100191, China
6 Department of Reproductive Endocrinology, Zhejiang Provincial People's Hospital, Hangzhou Medical College, Hangzhou 310014, China

Date of Submission01-Feb-2018
Date of Acceptance20-Aug-2018
Date of Web Publication26-Oct-2018

Correspondence Address:
Rong Li
Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing 100191, China; Key Laboratory of Assisted Reproduction, Ministry of Education, Beijing 100191, China

Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aja.aja_83_18

Rights and Permissions
  Abstract 


Anti-Müllerian hormone (AMH) is a functional marker of fetal Sertoli cells. The germ cell number in adults depends on the number of Sertoli cells produced during perinatal development. Recently, AMH has received increasing attention in research of disorders related to male fertility. This paper reviews and summarizes the articles on the regulation of AMH in males and the serum levels of AMH in male fertility-related disorders. We have determined that follicle-stimulating hormone (FSH) promotes AMH transcription in the absence of androgen signaling. Testosterone inhibits the transcriptional activation of AMH. The undetectable levels of serum AMH and testosterone levels indicate a lack of functional testicular tissue, for example, that in patients with anorchia or severe Klinefelter syndrome suffering from impaired spermatogenesis. The normal serum testosterone level and undetectable AMH are highly suggestive of persistent Müllerian duct syndrome (PMDS), combined with clinical manifestations. The levels of both AMH and testosterone are always subnormal in patients with mixed disorders of sex development (DSD). Mixed DSD is an early-onset complete type of disorder with fetal hypogonadism resulting from the dysfunction of both Leydig and Sertoli cells. Serum AMH levels are varying in patients with male fertility-related disorders, including pubertal delay, severe congenital hypogonadotropic hypogonadism, nonobstructive azoospermia, Klinefelter syndrome, varicocele, McCune-Albright syndrome, and male senescence.

Keywords: anti-Müllerian hormone; disorders related to male fertility; follicle-stimulating hormone; testosterone


How to cite this article:
Xu HY, Zhang HX, Xiao Z, Qiao J, Li R. Regulation of anti-Müllerian hormone (AMH) in males and the associations of serum AMH with the disorders of male fertility. Asian J Androl 2019;21:109-14

How to cite this URL:
Xu HY, Zhang HX, Xiao Z, Qiao J, Li R. Regulation of anti-Müllerian hormone (AMH) in males and the associations of serum AMH with the disorders of male fertility. Asian J Androl [serial online] 2019 [cited 2019 Aug 25];21:109-14. Available from: http://www.ajandrology.com/text.asp?2019/21/2/109/244249 - DOI: 10.4103/aja.aja_83_18

Hui-Yu Xu, Hong-Xian Zhang
These authors contributed equally to this work.





  Introduction to AMH Top


Anti-Müllerian hormone (AMH), also known as Müllerian-inhibiting substance (MIS), is a Sertoli cell-secreted protein that plays a major role in the development of internal male genitalia.[1] High expression of AMH in male gonads at the critical stage of embryonic genital development, i.e., 7 weeks of gestation,[2],[3] promotes regression of the Müllerian duct. In the absence of AMH, Müllerian ducts develop into female internal sex organs. Anti-Müllerian hormone is named based on these processes. AMH is a dimeric glycoprotein consisting of two identical 70-kDa subunits and constitutes the transforming growth factor-beta (TGF-β) superfamily together with inhibins, activins, bone morphogenetic proteins (BMPs), and growth differentiation factors (GDFs). TGF-β family members play important roles in the regulation of cell proliferation and apoptosis in many biological processes, including folliculogenesis and spermatogenesis.


  Role of AMH in Sertoli Cell Physiology Top


Sertoli cells are the earliest cell type that appear in the embryonic testis.[4],[5] More than 75% of the gonadal mass in the prepubertal testis is composed of Sertoli cells.[6],[7] Dysfunction of Sertoli cell proliferation or maturation may lead to secretory dysfunction via endocrine and paracrine signaling, leading to an inability to support spermatogenesis. During fetal life, AMH is exclusively secreted by Sertoli cells and can be used as a functional marker of fetal Sertoli cells.[1] Sertoli cells secrete other proteins that include (1) inhibins and activins, which are secreted by adult Sertoli cells to regulate follicle-stimulating hormone (FSH) production; (2) androgen-binding proteins (ABPs), which act as carrier proteins of testosterone and are responsible for the high concentration of intratesticular testosterone necessary for spermatogenesis;[8] (3) estradiol, which is transformed from testosterone catalyzed by aromatases in Sertoli cells; and (4) glial cell line-derived neurotrophic factors (GDNFs), which contribute to the self-renewal of spermatogonial stem cells. All of these factors secreted by Sertoli cells are involved in spermatogenesis.[9],[10],[11] Furthermore, Sertoli cells, rather than germ cells, express the androgen receptor,[11] which is critical for the regulation of spermatogenesis induced by high concentrations of intratesticular testosterone.[12]

FSH is responsible for AMH transcriptional activation and the increase of Sertoli cell number in the absence of androgen signaling

The germ cell number in adult men depends on the number of Sertoli cells produced during perinatal development.[5],[13] FSH has been recognized as a regulator of Sertoli cell number in developing testes.[14],[15] The hypothalamic–pituitary–gonadal (HPG) axis is inactive in prepuberty, as demonstrated by low levels of both testosterone and gonadotropins.[1],[16],[17],[18],[19] Lukas-Croisier et al.[20] used a prepubertal FSH-deficient (FSH-/-) transgenic male mouse model to demonstrate that FSH transcriptionally activates AMH production in the absence of androgen signaling. They showed that serum AMH concentration, Sertoli cell number, and testicular volume were decreased in FSH knockout mice and returned to normal after administration of recombinant FSH and transfection of FSH receptor plasmid. They next transfected different fragments of AMH promoter regions, together with the FSH receptor gene, into a prepubertal Sertoli cell line and added recombinant FSH protein to activate AMH transcription. The results showed that FSH transcriptionally activates AMH through a nonclassical cyclic adenosine monophosphate (cAMP) pathway by binding to the AMH promoter region located more than -1.9 kb away from the transcription initiation site at nuclear factor kappa-B (NF-κB) and transcription factor AP2-binding sites.[20] Unlike the distal regulation of the AMH promoter region by NF-κB, regulation of the proximal promoter of AMH has been extensively studied. Sex-determining region Y box 9 (Sox9),[21],[22] steroidogenic factor-1 (SF1),[23],[24],[25] and GATA factors[26],[27] are implicated in the transcriptional activation of AMH within -220 bp of the transcriptional start site independent of gonadotropic control.[28],[29] A schematic diagram of FSH-regulated AMH transcriptional activation is shown in [Figure 1]. Another study using Tfm mice with a mutation in the androgen receptor gene that made the XY mouse insensitive to androgens[30],[31] showed that FSH administration resulted in the elevation of serum AMH levels in the absence of androgen signaling.[32] FSH-induced AMH transcription and an increase in Sertoli cell number were also observed in neonates and adult humans suffering from hypogonadotropic hypogonadism (HH).[6],[16],[33] The androgen signaling pathway of these individuals is not functional, and their decreased AMH levels return to normal after the administration of recombinant FSH.
Figure 1: Schematic diagram of FSH-regulated AMH transcriptional activation. FSH: follicle-stimulating hormone; FSHR: FSH receptor; AC: adenylate cyclase; NF-κB: nuclear factor kappa-B; IκB: NF-κB inhibitor; SP1: transcription factor Sp1; GATA: GATA-binding proteins; SOX9: sex-determining region Y box 9; AMH: anti-Müllerian hormone; cAMP: cyclic adenosine monophosphate.

Click here to view


Testosterone downregulates AMH expression

The most obvious example of negative regulation of AMH by testosterone is that when boys enter puberty, a sudden increase in their testosterone levels results in decreased levels of AMH, indicating that testosterone has an inhibitory effect on AMH;[34] the increase in intratesticular testosterone levels is responsible for the inhibition of AMH levels.[32],[35],[36],[37] Another example is the increase in testosterone levels in precocious children, which is always accompanied by a decrease in AMH levels regardless of gonadotropin dependence or independence.[18] This negative regulatory pattern can also explain hormone levels in patients with androgen insensitivity syndrome (AIS) caused by mutations in the androgen receptor gene. The diagnosis of AIS is made by detecting normal-to-high testosterone and AMH levels and the absence of Müllerian derivatives in 46, XY males;[28],[38],[39],[40] the high levels of testosterone do not induce a decrease in AMH levels due to androgen signaling dysfunction.

Animal experiments also revealed a pattern of negative regulation between testosterone and AMH. The knockout of androgen receptors in Sertoli cells in mice induces a significant decrease in testosterone levels and thus gives rise to transiently elevated expression of AMH at both the mRNA and protein levels in Sertoli cells.[41] How does testosterone inhibit the expression of AMH? Another study performed the following mechanistic investigation to show that binding at the NF-κB-binding site in the distal promoter region of AMH provides transcriptional activity levels higher than those produced by binding at the SP1-, GATA-, and Sox9-binding sites in the proximal promoter regions.[20] Although there are no androgen receptor-binding sites in the AMH promoter region,[42] there are NF-κB binding sites, and NF-κB is negatively regulated by androgen receptors;[43],[44] therefore, although testosterone cannot directly regulate AMH transcription, it can fulfill its function by inhibiting the transcription of NF-κB and thus suppress the transcriptional activation of AMH.

However, AMH levels are not always negatively regulated by testosterone because of defects in androgen signaling. For instance, a synchronous increase in AMH and testosterone levels was discovered in neonates.[36],[45] It was discovered that the androgen receptor is present in fetal and neonatal Leydig and peritubular cells but not in Sertoli cells.[46],[47] The absence of androgen receptor expression in fetal and neonatal Sertoli cells may contribute to the lack of transcriptional suppression of AMH. Thus, FSH-induced AMH transcriptional activation and luteinizing hormone (LH)-induced testosterone activation account for the main biological events in fetal and neonate boys.


  Associations between Serum AMH and Disorders Related to Male Fertility Top


Diagnosis and differential diagnosis of disorders of sex development (DSD)

Male genital differentiation is driven by two hormones: testosterone, which is produced by fetal Leydig cells, maintains Wolffian ducts, and contributes to the virilization of external genitalia, and AMH, which is produced by fetal Sertoli cells and is responsible for the regression of fetal Müllerian ducts.[48] DSD in males may result from defects in the signaling of one or both of these hormones. Dysfunction of secretion or an inactive state of AMH, caused by mutations in AMH or its receptor AMHRII, leads to persistent Müllerian duct syndrome (PMDS). Patients with PMDS are born male according to the general human standard at birth, but the Müllerian duct derivatives persist, manifested as undescended testes (cryptorchidism) and the presence of a small, underdeveloped uterus in an XY infant or adult. Notably, fertility in PMDS patients is rare but possible if at least one testis descends to the scrotum with its excretory ducts intact.[49] No external genital ambiguity, especially without hypospadias, is the main feature of PMDS that distinguishes it from mixed gonadal dysgenesis, which is an early-onset complete type of DSD with fetal hypogonadism resulting from the dysfunction of both Leydig and Sertoli cells.[28]

Recently, mutations in the AMH and its receptor gene were found to account for 88% of PMDS cases in which undescended testes (UDTs) are the clinical manifestation.[49] The remaining 12% of PMDS cases are idiopathic, and no mutations in AMH or AMHRII have been detected. However, we cannot rule out the possibility of AMH or AMHRII mutations, as some studies have shown that the diversity of AMH or AMHRII mutations might be underrecognized and that the sensitivity and specificity of sequencing can be limited,[49] leading to unidentified mutations in the distal promoter or introns of AMH or AMHRII. Furthermore, we cannot rule out the possibility of mutations in other molecules in the AMH signaling pathway.

PMDS should be distinguished from other types of UDT. Leydig cell function in patients with PMDS is generally normal,[49] as indicated by normal levels of serum testosterone and LH.[17],[49] The levels of inhibin B, secreted by Sertoli cells,[50],[51],[52] are normal in boys with AMH mutations but undetectable in boys with AMHRII mutations.[17] Serum AMH levels depend on the molecular origin of AMH or AMHRII mutations. Very low or undetectable circulating AMH levels in prepubertal boys or adults with PMDS are characteristics of mutations in AMH, resulting in a lack of AMH protein secretion. Meanwhile, normal serum AMH levels are detected in boys with AMHRII mutations. Congenital adrenal hyperplasia (CAH) in females (46, XX) with a male phallus and bilateral nonpalpable gonads should first be differentially diagnosed from UDT via its severe complications, such as hyponatremia, hyperkalemia, and shock. When increasing severity of hypospadias with UDT is discovered, the possibility of a mixed DSD should be considered.[53] In patients with mixed types of DSD accompanied by low serum levels of both AMH and testosterone and external genital malformations, low AMH reflects severe testicular dysgenesis and should not be confused with PMDS. If an infant with bilateral nonpalpable testes has a 46, XY karyotype, an evaluation to distinguish anorchia from bilateral abdominal testes is needed to avoid surgical exploration. To assess the presence of testicular tissue, serum AMH should first be considered;[53] other hormone tests include those that detect FSH, LH, inhibin B, and testosterone levels.[53] A flowchart indicating the differential diagnosis of DSD is shown in [Figure 2].
Figure 2: AMH contributes to the differential diagnosis of DSD. UDT: undescended testis; CAH: congenital adrenal hyperplasia; DSD: disorders of sex development; PMDS: persistent Müllerian duct syndrome; AMH: anti-Müllerian hormone; T: testosterone; AMHR: AMH receptor.

Click here to view


Studies of unilateral UDT revealed that UDTs in children are smaller than their descended counterparts (P < 0.001).[54],[55] Given that Sertoli cells account for 75% of testis mass in prepubertal males,[6],[7] there may be varying degrees of decline in the number of Sertoli cells in UDT, which may result from increased temperature around the UDT. The degree of AMH decrease in boys bearing cryptorchidism is related to the severity of UDT injury,[56],[57],[58] suggesting that deteriorated Sertoli cell function may be an early example of damage from UDT. Moreover, infertility is the major long-term concern of patients with a history of UDT.[53] Infertility risks of 30% and 54% were discovered in unilateral and bilateral UDT, respectively,[59],[60],[61],[62],[63] in accordance with the duration for which UDT is exposed to abdominal temperature. A 75%–100% risk of infertility was found in boys with bilateral UDT in whom no germ cells were found on biopsy.[64] In conclusion, the degree of male infertility caused by UDT is related to the severity of injury to Sertoli cells; thus, a higher degree of serum decline in AMH in boys may suggest a greater risk of infertility when they become adults.

Distinguishing pubertal delay from congenital hypogonadotropic hypogonadism

Constitutional pubertal delay and congenital HH share the same clinical manifestation of delayed sexual maturation in prepubertal boys. Levels of gonadotropin and testosterone are very low in prepubertal boys and therefore have little clinical significance; thus, AMH, the marker of Sertoli cells, is of great importance in the differential diagnosis of constitutional pubertal delay and congenital HH.[18],[46]

Congenital HH is often accompanied by Sertoli cell dysfunction.[65] Severe deficiency in gonadotropin levels in congenital HH patients results in a decreased number of Sertoli cells and correspondingly low levels of AMH and inhibin B.[65],[66],[67] The constitutional delay of puberty reflects a eugonadal state of Sertoli cells, and serum AMH is within the normal level for prepubertal boys.[68] In patients with untreated congenital HH, the AMH level is increased upon administration of recombinant FSH due to FSH-induced proliferation of Sertoli cells, whereas further treatment with human chorionic gonadotropin (hCG) gives rise to a decline in AMH levels due to the hCG-induced increased levels of testosterone, which induces inhibition of AMH that overrides FSH-initiated AMH transcription. However, the administration of exogenous testosterone did not result in a decrease in AMH concentrations, which may be caused by low intratesticular testosterone levels in congenital HH patients.

Nonobstructive azoospermia and Klinefelter syndrome (47, XXY)

Nonobstructive azoospermia (NOA) is the most severe type of male infertility, characterized by a lack of sperm in semen induced by impaired spermatogenesis.[69] Increased serum FSH, decreased serum AMH and inhibin B, have been discovered in men with NOA.[70],[71],[72] With the advent of intracytoplasmic sperm injection (ICSI) technology, these NOA patients also have the opportunity to have their own children through testicular sperm extraction (TESE) or microdissection-testicular sperm extraction (MD-TESE), with sperm recovery rates (SRRs) of only 40%–60%.[69],[73] Currently, there are no acknowledged markers of SRR with good sensitivity and specificity. FSH, inhibin B, AMH, and testosterone, although differentially expressed in NOA, are not good predictors of SRR. Higher baseline testosterone,[74] lower FSH,[75] higher AMH,[76] or higher inhibin B[77] levels do not guarantee a better SRR in NOA patients. The underlying mechanism may be the following: the function of the Sertoli cells and interstitial cells is impaired, as indicated by abnormal hormone levels, but not completely lost in a large number of NOA patients; spermatogenesis is only present in small areas, if any.[78] In our clinical practice, we have identified a certain number of NOA patients whose serum AMH levels are below the lower limit of the male reference interval or even undetectable and whose serum testosterone levels are normal or subnormal yet obtain good pregnancy outcomes using their own sperm retrieved via TESE or MD-TESE. These serum markers may be useful when combined with testicular volume, age and other markers to predict SRR before TESE or MD-TESE using a multivariable regression method.[77],[79]

Klinefelter syndrome is characterized by accelerated germ cell depletion[80] and occurs in approximately 10%–12% of NOA men.[81] In patients with Klinefelter syndrome, circulating AMH levels are within the reference range until puberty; thereafter, AMH declines to subnormal concentrations in adults.[82],[83] In a 12.3-year follow-up study of 29 patients with Klinefelter syndrome, an early increase in FSH was detected, accompanied by abnormally low or undetectable levels of AMH and inhibin B in advanced pubertal stages, which may be explained by progressive impairment of endocrine function during childhood and puberty.[83] However, a delay in the puberty-related decline of AMH was observed in patients with Klinefelter syndrome, finally leading to decreased AMH levels in adulthood,[82] which may be caused by temporary functional compensation of Sertoli cells. Furthermore, in our clinical practice, we identified a few severe NOA patients, including severe Klinefelter syndrome patients, whose serum AMH and testosterone levels were both undetectable and with no sperm retrieved via MD-TESE, indicating that their germ cells were completely depleted. Undetectable AMH and testosterone were also used to distinguish anorchia from UDT,[84],[85],[86] as shown in [Figure 2], implying that in male adults, undetectable serum AMH and testosterone can be used to assess whether any functional testicular tissue or, specifically, functional germ cells exist.

Varicocele

Varicocele is an abnormal enlargement and bending of the pampiniform venous plexus in the scrotum. The adverse effects of varicocele on spermatogenesis are progressive and therefore decrease male fertility with time. Expansion of the veins impairs the testicular blood supply, resulting in a reduction in the oxygenated blood and nutrient supply to the local testis, which leads to a decline in the quality and quantity of sperm; on the other hand, it also induces dysfunction of the testicular nervous plexus, the main function of which is to regulate testicular temperature. Higher testicular temperatures can lead to testicular atrophy and infertility. Indeed, varicocele is the main cause of male infertility,[87] and it was found in approximately 35% of primary infertile men and 81% of secondary infertile men.[88]

The severe damage caused by varicocele is correlated with impaired function of Sertoli cells. According to the study from Li et al.,[89] the levels of transferrins and androgen-binding proteins secreted by Sertoli cells were reported to be downregulated in patients suffering from varicocele, suggesting that decreased testicular blood flow may lead to impaired function of Sertoli cells. Furthermore, testicular biopsies in patients with varicocele showed that the germ cells in the seminiferous tubule were sloughed, and this phenomenon was often associated with impaired Sertoli cell function.[90]

An analysis of serum AMH levels in varicocele-bearing patients was inconclusive. A study in adult subfertility men including varicocele, idiopathic NOA, idiopathic nonobstructive dyspermia, cryptorchidism, and other diagnoses indicated that circulating AMH levels in subfertile men were 60% lower than those in corresponding controls, accompanied by a decreased level of inhibin B, indicating the decreased function of Sertoli cells in varicocele-bearing adult patients.[91] In prepubertal and pubertal boys with varicocele, AMH concentrations were elevated, accompanied by an increase in inhibin B levels, suggesting a compensatory increase in Sertoli cell function in the early-onset varicocele.[92] There was also an article reporting a lower concentration of AMH in the local spermatic vein than in the peripheral blood, suggesting that poor blood supply in patients with varicocele causes the deterioration of Sertoli cell function.[93]

McCune-Albright syndrome in boys

As we mentioned previously, normal puberty is accompanied by decreased serum levels of AMH. However, in boys with McCune-Albright syndrome, precocious puberty is observed, but abnormal increased instead of decreased levels of AMH are detected,[94],[95],[96] accompanied by macro-orchidism and androgen-dependent secondary sexual defects. Hyperfunction of Sertoli cells without Leydig cell activation was reported to be responsible for the onset of this disease.[97]

Male senescence

Testes, hormone production, and spermatogenesis undergo senescence as a man ages.[98] Johnson et al.[99] identified an age-related decrease in Sertoli cell number; consistent with this, AMH, as a marker of immature Sertoli cells, was also found to be reduced with increasing age[36],[100],[101] and negatively correlated with FSH and LH, which indicates that decreased AMH levels as a man ages represent age-related reduced Sertoli cell function.


  Conclusion Top


In the absence of androgen signaling, FSH promotes AMH transcription by activating the -1.9 kb AMH promoter region, where NF-κB has the highest level of transcriptional activation activity, and the proximal within -220 bp[20]AMH promoter region, where Sox9,[21],[22] SF1,[23],[24],[25] and GATA factors[25],[26],[27] reside. Testosterone inhibits the transcriptional activation of AMH, hypothetically through transcriptional inhibition of NF-κB. Regarding the associations between serum AMH and disorders related to male fertility, undetectable serum AMH and testosterone indicate a lack of functional testicular tissue, for example, that in patients with anorchia or severe Klinefelter syndrome suffering from impaired spermatogenesis. Normal serum testosterone levels and undetectable AMH are highly suggestive of PMDS. The levels of both AMH and testosterone are always subnormal in patients with mixed DSD (as shown in [Figure 2]). The usefulness of AMH levels in these conditions (pubertal delay, severe congenital HH, NOA, Klinefelter, varicocele, McCune-Albright syndrome, and male senescence) is also summarized, as indicated in [Table 1].
Table 1: Anti-Müllerian hormone levels in disorders related to male fertility

Click here to view



  Author Contributions Top


HYX and HXZ participated in the study design and references collection, and most of the manuscript writing. ZX participated in Figures drawing. JQ conceived the study. RL conceived and designed the study, edited the manuscript, and finally approved the final version. All authors read and approved the final manuscript.


  Competing Interests Top


The authors declare no competing interests.



 
  References Top

1.
Tran D, Muesy-Dessole N, Josso N. Anti-Müllerian hormone is a functional marker of foetal sertoli cells. Nature 1977; 269: 411–2.  Back to cited text no. 1
    
2.
Damiani D, Mascolli MA, Almeida MJ, Jaubert F, Fellous M, et al. Persistence of Müllerian remnants in complete androgen insensitivity syndrome. J Pediatr Endocrinol Metab 2002; 15: 1553–6.  Back to cited text no. 2
    
3.
Josso N, Lamarre I, Picard JY, Berta P, Davies N, et al. Anti-Müllerian hormone in early human development. Early Hum Dev 1993; 33: 91–9.  Back to cited text no. 3
    
4.
Palmer SJ, Burgoyne PS. In situ analysis of fetal, prepuberal and adult XX–XY chimaeric mouse testes: Sertoli cells are predominantly, but not exclusively, XY. Development 1991; 112: 265–8.  Back to cited text no. 4
    
5.
Griswold MD. The central role of sertoli cells in spermatogenesis. Semin Cell Dev Biol 1998; 9: 411–6.  Back to cited text no. 5
    
6.
Young J, Chanson P, Salenave S, Noel M, Brailly S, et al. Testicular anti-Müllerian hormone secretion is stimulated by recombinant human FSH in patients with congenital hypogonadotropic hypogonadism. J Clin Endocrinol Metab 2005; 90: 724–8.  Back to cited text no. 6
    
7.
Nistal M, Abaurrea MA, Paniagua R. Morphological and histometric study on the human sertoli cell from birth to the onset of puberty. J Anat 1982; 134: 351–63.  Back to cited text no. 7
    
8.
Neto FT, Bach PV, Najari BB, Li PS, Goldstein M. Spermatogenesis in humans and its affecting factors. Semin Cell Dev Biol 2016; 59: 10–26.  Back to cited text no. 8
    
9.
Correia S, Cardoso HJ, Cavaco JE, Socorro S. Oestrogens as apoptosis regulators in mammalian testis: angels or devils? Expert Rev Mol Med 2015; 17: e2.  Back to cited text no. 9
    
10.
Robertson DM. Inhibin and male. In: Reference Module in Biomedical Sciences. Cambridge: Elsevier; 2018.  Back to cited text no. 10
    
11.
Erwin Goldberg BR. Spermatogenesis: overview. In: Reference Module in Biomedical Sciences. Massachusetts: Elsevier; 2018.  Back to cited text no. 11
    
12.
Ohlander SJ, Lindgren MC, Lipshultz LI. Testosterone and male infertility. Urol Clin North Am 2016; 43: 195–202.  Back to cited text no. 12
    
13.
Orth JM, Gunsalus GL, Lamperti AA. Evidence from sertoli cell-depleted rats indicates that spermatid number in adults depends on numbers of sertoli cells produced during perinatal development. Endocrinology 1988; 122: 787–94.  Back to cited text no. 13
    
14.
Orth JM. FSH-induced Sertoli cell proliferation in the developing rat is modified by beta-endorphin produced in the testis. Endocrinology 1986; 119: 1876–8.  Back to cited text no. 14
    
15.
Johnston H, Baker PJ, Abel M, Charlton HM, Jackson G, et al. Regulation of sertoli cell number and activity by follicle-stimulating hormone and androgen during postnatal development in the mouse. Endocrinology 2004; 145: 318–29.  Back to cited text no. 15
    
16.
Grinspon RP, Rey RA. Anti-Müllerian hormone and sertoli cell function in paediatric male hypogonadism. Horm Res Paediatr 2010; 73: 81–92.  Back to cited text no. 16
    
17.
Lindhardt Johansen M, Hagen CP, Johannsen TH, Main KM, Picard JY, et al. Anti-Müllerian hormone and its clinical use in pediatrics with special emphasis on disorders of sex development. Int J Endocrinol 2013; 2013: 198698.  Back to cited text no. 17
    
18.
Edelsztein NY, Grinspon RP, Schteingart HF, Rey RA. Anti-Müllerian hormone as a marker of steroid and gonadotropin action in the testis of children and adolescents with disorders of the gonadal axis. Int J Pediatr Endocrinol 2016; 2016: 20.  Back to cited text no. 18
    
19.
Grinspon RP, Ropelato MG, Bedecarras P, Loreti N, Ballerini MG, et al. Gonadotrophin secretion pattern in anorchid boys from birth to pubertal age: pathophysiological aspects and diagnostic usefulness. Clin Endocrinol (Oxf) 2012; 76: 698–705.  Back to cited text no. 19
    
20.
Lukas-Croisier C, Lasala C, Nicaud J, Bedecarras P, Kumar TR, et al. Follicle-stimulating hormone increases testicular anti-Müllerian hormone (AMH) production through sertoli cell proliferation and a nonclassical cyclic adenosine 5'-monophosphate-mediated activation of the AMH gene. Mol Endocrinol 2003; 17: 550–61.  Back to cited text no. 20
    
21.
De Santa Barbara P, Bonneaud N, Boizet B, Desclozeaux M, Moniot B, et al. Direct interaction of SRY-related protein SOX9 and steroidogenic factor 1 regulates transcription of the human anti-Müllerian hormone gene. Mol Cell Biol 1998; 18: 6653–65.  Back to cited text no. 21
    
22.
Arango NA, Lovell-Badge R, Behringer RR. Targeted mutagenesis of the endogenous mouse Mis gene promoter: in vivo definition of genetic pathways of vertebrate sexual development. Cell 1999; 99: 409–19.  Back to cited text no. 22
    
23.
Shen WH, Moore CC, Ikeda Y, Parker KL, Ingraham HA. Nuclear receptor steroidogenic factor 1 regulates the Müllerian inhibiting substance gene: a link to the sex determination cascade. Cell 1994; 77: 651–61.  Back to cited text no. 23
    
24.
Giuili G, Shen WH, Ingraham HA. The nuclear receptor SF-1 mediates sexually dimorphic expression of Müllerian inhibiting substance, in vivo. Development 1997; 124: 1799–807.  Back to cited text no. 24
    
25.
Watanabe K, Clarke TR, Lane AH, Wang X, Donahoe PK. Endogenous expression of Müllerian inhibiting substance in early postnatal rat sertoli cells requires multiple steroidogenic factor-1 and GATA-4-binding sites. Proc Natl Acad Sci U S A 2000; 97: 1624–9.  Back to cited text no. 25
    
26.
Tremblay JJ, Viger RS. Transcription factor GATA-4 enhances Müllerian inhibiting substance gene transcription through a direct interaction with the nuclear receptor SF-1. Mol Endocrinol 1999; 13: 1388–401.  Back to cited text no. 26
    
27.
Beau C, Rauch M, Joulin V, Jegou B, Guerrier D. GATA-1 is a potential repressor of anti-Müllerian hormone expression during the establishment of puberty in the mouse. Mol Reprod Dev 2000; 56: 124–38.  Back to cited text no. 27
    
28.
Rey RA, Grinspon RP. Normal male sexual differentiation and aetiology of disorders of sex development. Best Pract Res Clin Endocrinol Metab 2011; 25: 221–38.  Back to cited text no. 28
    
29.
Rey R, Lukas-Croisier C, Lasala C, Bedecarras P. AMH/MIS: what we know already about the gene, the protein and its regulation. Mol Cell Endocrinol 2003; 211: 21–31.  Back to cited text no. 29
    
30.
Lyon MF, Hawkes SG. X-linked gene for testicular feminization in the mouse. Nature 1970; 227: 1217–9.  Back to cited text no. 30
    
31.
Charest NJ, Zhou ZX, Lubahn DB, Olsen KL, Wilson EM, et al. A frameshift mutation destabilizes androgen receptor messenger RNA in the Tfm mouse. Mol Endocrinol 1991; 5: 573–81.  Back to cited text no. 31
    
32.
Al-Attar L, Noel K, Dutertre M, Belville C, Forest MG, et al. Hormonal and cellular regulation of sertoli cell anti-Müllerian hormone production in the postnatal mouse. J Clin Invest 1997; 100: 1335–43.  Back to cited text no. 32
    
33.
Bougneres P, Francois M, Pantalone L, Rodrigue D, Bouvattier C, et al. Effects of an early postnatal treatment of hypogonadotropic hypogonadism with a continuous subcutaneous infusion of recombinant follicle-stimulating hormone and luteinizing hormone. J Clin Endocrinol Metab 2008; 93: 2202–5.  Back to cited text no. 33
    
34.
Rey R, Lordereau-Richard I, Carel JC, Barbet P, Cate RL, et al. Anti-mullerian hormone and testosterone serum levels are inversely during normal and precocious pubertal development. J Clin Endocrinol Metab 1993; 77: 1220–6.  Back to cited text no. 34
    
35.
Young J, Rey R, Couzinet B, Chanson P, Josso N, et al. Anti-Müllerian hormone in patients with hypogonadotropic hypogonadism. J Clin Endocrinol Metab 1999; 84: 2696–9.  Back to cited text no. 35
    
36.
Aksglaede L, Sorensen K, Boas M, Mouritsen A, Hagen CP, et al. Changes in anti-Müllerian hormone (AMH) throughout the life span: a population-based study of 1027 healthy males from birth (cord blood) to the age of 69 years. J Clin Endocrinol Metab 2010; 95: 5357–64.  Back to cited text no. 36
    
37.
Grinspon RP, Bedecarras P, Ballerini MG, Iniguez G, Rocha A, et al. Early onset of primary hypogonadism revealed by serum anti-Müllerian hormone determination during infancy and childhood in trisomy 21. Int J Androl 2011; 34: e487–98.  Back to cited text no. 37
    
38.
Josso N, Rey R, Picard JY. Testicular anti-Müllerian hormone: clinical applications in DSD. Semin Reprod Med 2012; 30: 364–73.  Back to cited text no. 38
    
39.
Werner R, Grotsch H, Hiort O. 46, XY disorders of sex development – the undermasculinised male with disorders of androgen action. Best Pract Res Clin Endocrinol Metab 2010; 24: 263–77.  Back to cited text no. 39
    
40.
Bukhari I, Li G, Wang L, Iqbal F, Zhang H, et al. Effects of androgen receptor mutation on testicular histopathology of patient having complete androgen insensitivity. J Mol Histol 2017; 48: 159–67.  Back to cited text no. 40
    
41.
Chang C, Chen YT, Yeh SD, Xu Q, Wang RS, et al. Infertility with defective spermatogenesis and hypotestosteronemia in male mice lacking the androgen receptor in sertoli cells. Proc Natl Acad Sci U S A 2004; 101: 6876–81.  Back to cited text no. 41
    
42.
Rey R, Josso N. Regulation of testicular anti-Müllerian hormone secretion. Eur J Endocrinol 1996; 135: 144–52.  Back to cited text no. 42
    
43.
McKay LI, Cidlowski JA. Molecular control of immune/inflammatory responses: interactions between nuclear factor-kappa B and steroid receptor-signaling pathways. Endocr Rev 1999; 20: 435–59.  Back to cited text no. 43
    
44.
McKay LI, Cidlowski JA. Cross-talk between nuclear factor-kappa B and the steroid hormone receptors: mechanisms of mutual antagonism. Mol Endocrinol 1998; 12: 45–56.  Back to cited text no. 44
    
45.
Corbier P, Edwards DA, Roffi J. The neonatal testosterone surge: a comparative study. Arch Int Physiol Biochim Biophys 1992; 100: 127–31.  Back to cited text no. 45
    
46.
Matuszczak E, Hermanowicz A, Komarowska M, Debek W. Serum AMH in physiology and pathology of male gonads. Int J Endocrinol 2013; 2013: 128907.  Back to cited text no. 46
    
47.
Chemes HE, Rey RA, Nistal M, Regadera J, Musse M, et al. Physiological androgen insensitivity of the fetal, neonatal, and early infantile testis is explained by the ontogeny of the androgen receptor expression in sertoli cells. J Clin Endocrinol Metab 2008; 93: 4408–12.  Back to cited text no. 47
    
48.
Jost A. Problems of fetal endocrinology: the gonadal and hypophyseal hormones. Recent Prog Horm Res 1953; 8: 379–418.  Back to cited text no. 48
    
49.
Picard JY, Cate RL, Racine C, Josso N. The persistent Müllerian duct syndrome: an update based upon a personal experience of 157 cases. Sex Dev 2017; 11: 109–25.  Back to cited text no. 49
    
50.
Anawalt BD, Bebb RA, Matsumoto AM, Groome NP, Illingworth PJ, et al. Serum inhibin B levels reflect sertoli cell function in normal men and men with testicular dysfunction. J Clin Endocrinol Metab 1996; 81: 3341–5.  Back to cited text no. 50
    
51.
Iliadou PK, Tsametis C, Kaprara A, Papadimas I, Goulis DG. The sertoli cell: novel clinical potentiality. Hormones (Athens) 2015; 14: 504–14.  Back to cited text no. 51
    
52.
Hipler UC, Hochheim B, Knoll B, Tittelbach J, Schreiber G. Serum inhibin B as a marker for spermatogenesis. Arch Androl 2001; 46: 217–22.  Back to cited text no. 52
    
53.
Kolon TF, Herndon CD, Baker LA, Baskin LS, Baxter CG, et al. Evaluation and treatment of cryptorchidism: AUA guideline. J Urol 2014; 192: 337–45.  Back to cited text no. 53
    
54.
Kollin C, Granholm T, Nordenskjold A, Ritzen EM. Growth of spontaneously descended and surgically treated testes during early childhood. Pediatrics 2014; 131: e1174–80.  Back to cited text no. 54
    
55.
van der Plas EM, Zijp GW, Froeling FM, van der Voort-Doedens LM, Meij-de Vries A, et al. Long-term testicular volume after orchiopexy at diagnosis of acquired undescended testis. J Urol 2013; 190: 257–62.  Back to cited text no. 55
    
56.
Matuszczak E, Hermanowicz A, Debek W, Oksiuta M, Dzienis-Koronkiewicz E, et al. Serum AMH concentration as a marker evaluating gonadal function in boys operated on for unilateral cryptorchidism between 1st and 4th year of life. Endocrine 2012; 41: 334–7.  Back to cited text no. 56
    
57.
Demircan M, Akinci A, Mutus M. The effects of orchiopexy on serum anti-Müllerian hormone levels in unilateral cryptorchid infants. Pediatr Surg Int 2006; 22: 271–3.  Back to cited text no. 57
    
58.
Guibourdenche J, Lucidarme N, Chevenne D, Rigal O, Nicolas M, et al. Anti-Müllerian hormone levels in serum from human foetuses and children: pattern and clinical interest. Mol Cell Endocrinol 2003; 211: 55–63.  Back to cited text no. 58
    
59.
Cortes D. Cryptorchidism–aspects of pathogenesis, histology and treatment. Scand J Urol Nephrol Suppl 1998; 196: 1–54.  Back to cited text no. 59
    
60.
Engeler DS, Hosli PO, John H, Bannwart F, Sulser T, et al. Early orchiopexy: prepubertal intratubular germ cell neoplasia and fertility outcome. Urology 2000; 56: 144–8.  Back to cited text no. 60
    
61.
Lee PA, O'Leary LA, Songer NJ, Coughlin MT, Bellinger MF, et al. Paternity after unilateral cryptorchidism: a controlled study. Pediatrics 1996; 98: 676–9.  Back to cited text no. 61
    
62.
Thorup J, McLachlan R, Cortes D, Nation TR, Balic A, et al. What is new in cryptorchidism and hypospadias – a critical review on the testicular dysgenesis hypothesis. J Pediatr Surg 2010; 45: 2074–86.  Back to cited text no. 62
    
63.
Lee PA, Coughlin MT. Fertility after bilateral cryptorchidism. Evaluation by paternity, hormone, and semen data. Horm Res 2001; 55: 28–32.  Back to cited text no. 63
    
64.
Cortes D, Thorup JM, Beck BL. Quantitative histology of germ cells in the undescended testes of human fetuses, neonates and infants. J Urol 1995; 154: 1188–92.  Back to cited text no. 64
    
65.
Hero M, Tommiska J, Vaaralahti K, Laitinen EM, Sipila I, et al. Circulating antimüllerian hormone levels in boys decline during early puberty and correlate with inhibin B. Fertil Steril 2012; 97: 1242–7.  Back to cited text no. 65
    
66.
Rey RA, Grinspon RP, Gottlieb S, Pasqualini T, Knoblovits P, et al. Male hypogonadism: an extended classification based on a developmental, endocrine physiology-based approach. Andrology 2013; 1: 3–16.  Back to cited text no. 66
    
67.
Coutant R, Biette-Demeneix E, Bouvattier C, Bouhours-Nouet N, Gatelais F, et al. Baseline inhibin B and anti-Müllerian hormone measurements for diagnosis of hypogonadotropic hypogonadism (HH) in boys with delayed puberty. J Clin Endocrinol Metab 2010; 95: 5225–32.  Back to cited text no. 67
    
68.
Adan L, Lechevalier P, Couto-Silva AC, Boissan M, Trivin C, et al. Plasma inhibin B and antimüllerian hormone concentrations in boys: discriminating between congenital hypogonadotropic hypogonadism and constitutional pubertal delay. Med Sci Monit 2010; 16: CR511–7.  Back to cited text no. 68
    
69.
Klami R, Mankonen H, Perheentupa A. Successful microdissection testicular sperm extraction for men with non-obstructive azoospermia. Reprod Biol 2018; 18: 137–42.  Back to cited text no. 69
    
70.
Madani AH, Falahatkar S, Heidarzadeh A, Roshan ZA, Sazgari E, et al. Sensitivity and specificity of serum FSH and testis size in predicting the existence of spermatogenesis in azoospermic infertile men. Andrologia 2012; 44: 205–9.  Back to cited text no. 70
    
71.
Esteves SC, Miyaoka R, Agarwal A. An update on the clinical assessment of the infertile male. [corrected]. Clinics (Sao Paulo) 2011; 66: 691–700.  Back to cited text no. 71
    
72.
La Marca A, Pati M, Orvieto R, Stabile G, Carducci Artenisio A, et al. Serum anti-Müllerian hormone levels in women with secondary amenorrhea. Fertil Steril 2006; 85: 1547–9.  Back to cited text no. 72
    
73.
Dabaja AA, Schlegel PN. Microdissection testicular sperm extraction: an update. Asian J Androl 2013; 15: 35–9.  Back to cited text no. 73
    
74.
Althakafi SA, Mustafa OM, Seyam RM, Al-Hathal N, Kattan S. Serum testosterone levels and other determinants of sperm retrieval in microdissection testicular sperm extraction. Transl Androl Urol 2017; 6: 282–7.  Back to cited text no. 74
    
75.
Li H, Chen LP, Yang J, Li MC, Chen RB, et al. Predictive value of FSH, testicular volume, and histopathological findings for the sperm retrieval rate of microdissection TESE in nonobstructive azoospermia: a meta-analysis. Asian J Androl 2018; 20: 30–6.  Back to cited text no. 75
    
76.
Isikoglu M, Ozgur K, Oehninger S, Ozdem S, Seleker M. Serum anti-Müllerian hormone levels do not predict the efficiency of testicular sperm retrieval in men with non-obstructive azoospermia. Gynecol Endocrinol 2006; 22: 256–60.  Back to cited text no. 76
    
77.
Cissen M, Meijerink AM, D'Hauwers KW, Meissner A, van der Weide N, et al. Prediction model for obtaining spermatozoa with testicular sperm extraction in men with non-obstructive azoospermia. Hum Reprod 2016; 31: 1934–41.  Back to cited text no. 77
    
78.
Schlegel PN. Testicular sperm extraction: microdissection improves sperm yield with minimal tissue excision. Hum Reprod 1999; 14: 131–5.  Back to cited text no. 78
    
79.
Ramasamy R, Padilla WO, Osterberg EC, Srivastava A, Reifsnyder JE, et al. A comparison of models for predicting sperm retrieval before microdissection testicular sperm extraction in men with nonobstructive azoospermia. J Urol 2013; 189: 638–42.  Back to cited text no. 79
    
80.
Wikstrom AM, Raivio T, Hadziselimovic F, Wikstrom S, Tuuri T, et al. Klinefelter syndrome in adolescence: onset of puberty is associated with accelerated germ cell depletion. J Clin Endocrinol Metab 2004; 89: 2263–70.  Back to cited text no. 80
    
81.
Forti G, Corona G, Vignozzi L, Krausz C, Maggi M. Klinefelter's syndrome: a clinical and therapeutical update. Sex Dev 2010; 4: 249–58.  Back to cited text no. 81
    
82.
Aksglaede L, Christiansen P, Sorensen K, Boas M, Linneberg A, et al. Serum concentrations of anti-Müllerian hormone (AMH) in 95 patients with Klinefelter syndrome with or without cryptorchidism. Acta Paediatr 2011; 100: 839–45.  Back to cited text no. 82
    
83.
Bastida MG, Rey RA, Bergada I, Bedecarras P, Andreone L, et al. Establishment of testicular endocrine function impairment during childhood and puberty in boys with Klinefelter syndrome. Clin Endocrinol (Oxf) 2007; 67: 863–70.  Back to cited text no. 83
    
84.
Lee MM, Misra M, Donahoe PK, MacLaughlin DT. MIS/AMH in the assessment of cryptorchidism and intersex conditions. Mol Cell Endocrinol 2003; 211: 91–8.  Back to cited text no. 84
    
85.
Stoppa-Vaucher S, Djemli A, Van Vliet G. Undetectable AMH at 3 days of age: a clue to bilateral anorchia. Clin Biochem 2010; 43: 1373–4.  Back to cited text no. 85
    
86.
Szarras-Czapnik M, Gajewska M, Ksiazyk J, Janas R, Ginalska-Malinowska M. [Anti-Müllerian hormone (AMH) measurements in the assessment of testicular function in prepubertal boys and in sexual differentiation disorders]. Endokrynol Diabetol Chor Przemiany Materii Wieku Rozw 2006; 12: 195–9. [Article in Polish].  Back to cited text no. 86
    
87.
Redmon JB, Carey P, Pryor JL. Varicocele–the most common cause of male factor infertility? Hum Reprod Update 2002; 8: 53–8.  Back to cited text no. 87
    
88.
Gorelick JI, Goldstein M. Loss of fertility in men with varicocele. Fertil Steril 1993; 59: 613–6.  Back to cited text no. 88
    
89.
Li H, Dubocq F, Jiang Y, Tiguert R, Gheiler EL, et al. Effect of surgically induced varicocele on testicular blood flow and sertoli cell function. Urology 1999; 53: 1258–62.  Back to cited text no. 89
    
90.
Cameron DF, Snydle FE, Ross MH, Drylie DM. Ultrastructural alterations in the adluminal testicular compartment in men with varicocele. Fertil Steril 1980; 33: 526–33.  Back to cited text no. 90
    
91.
Goulis DG, Iliadou PK, Tsametis C, Gerou S, Tarlatzis BC, et al. Serum anti-Müllerian hormone levels differentiate control from subfertile men but not men with different causes of subfertility. Gynecol Endocrinol 2008; 24: 158–60.  Back to cited text no. 91
    
92.
Trigo RV, Bergada I, Rey R, Ballerini MG, Bedecarras P, et al. Altered serum profile of inhibin B, Pro-alphaC and anti-Müllerian hormone in prepubertal and pubertal boys with varicocele. Clin Endocrinol (Oxf) 2004; 60: 758–64.  Back to cited text no. 92
    
93.
Goulis D, Mintziori G, Koliakos N, Hatzichristou D, Papadimas I, et al. Inhibin B and anti-Müllerian hormone in spermatic vein of subfertile men with varicocele. Reprod Sci 2011; 18: 551–5.  Back to cited text no. 93
    
94.
Volkl TM, Dorr HG. McCune-Albright syndrome: clinical picture and natural history in children and adolescents. J Pediatr Endocrinol Metab 2006; 19 Suppl 2: 551–9.  Back to cited text no. 94
    
95.
Coutant R, Lumbroso S, Rey R, Lahlou N, Venara M, et al. Macroorchidism due to autonomous hyperfunction of sertoli cells and G(s)alpha gene mutation: an unusual expression of McCune-Albright syndrome in a prepubertal boy. J Clin Endocrinol Metab 2001; 86: 1778–81.  Back to cited text no. 95
    
96.
Mamkin I, Philibert P, Anhalt H, Ten S, Sultan C. Unusual phenotypical variations in a boy with McCune-Albright syndrome. Horm Res Paediatr 2010; 73: 215–22.  Back to cited text no. 96
    
97.
Rey RA, Venara M, Coutant R, Trabut JB, Rouleau S, et al. Unexpected mosaicism of R201H-GNAS1 mutant-bearing cells in the testes underlie macro-orchidism without sexual precocity in McCune-Albright syndrome. Hum Mol Genet 2006; 15: 3538–43.  Back to cited text no. 97
    
98.
Gunes S, Hekim GN, Arslan MA, Asci R. Effects of aging on the male reproductive system. J Assist Reprod Genet 2016; 33: 441–54.  Back to cited text no. 98
    
99.
Johnson L, Petty CS, Neaves WB. Age-related variation in seminiferous tubules in men. A stereologic evaluation. J Androl 1986; 7: 316–22.  Back to cited text no. 99
    
100.
Chong YH, Dennis NA, Connolly MJ, Teh R, Jones GT, et al. Elderly men have low levels of anti-Müllerian hormone and inhibin B, but with high interpersonal variation: a cross-sectional study of the sertoli cell hormones in 615 community-dwelling men. PLoS One 2013; 8: e70967.  Back to cited text no. 100
    
101.
Ramezani Tehrani F, Mansournia MA, Solaymani-Dodaran M, Minooee S, Azizi F. Serum variations of anti-Müllerian hormone and total testosterone with aging in healthy adult Iranian men: a population-based study. PLoS One 2017; 12: e0179634.  Back to cited text no. 101
    


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1]


This article has been cited by
1 Derivation of reference intervals for Antimüllerian hormone, specific for russian population25
I. I. Guzov,E. Yu. Pecherina,A. V. Ruzhanskaya,V. A. Kozlov,O. I. Laskina,N. N. Sintyrina,E. A. Sedyshkina,E. Yu. Gvozdik,S. A. Tye,A. V. Zenkina,A. S. Kurgannikov
Laboratornaya sluzhba. 2019; 8(2): 25
[Pubmed] | [DOI]
2 A new panel containing specific spermatogenesis markers to identify spermatogenic cells in nonobstructive azoospermia patients
Xinxi Zhao,Yiqin Wang,Meng Ma,Wei Zhang,Jiqiang Si,Wei Wang,Zhen Lin,Gang Han,Charlie Degui Chen,Minghan Tong,Yanping Kuang,Qifeng Lyu
Acta Biochimica et Biophysica Sinica. 2019; 51(6): 656
[Pubmed] | [DOI]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction to AMH
Role of AMH in S...
Associations bet...
Conclusion
Author Contributions
Competing Interests
References
Article Figures
Article Tables

 Article Access Statistics
    Viewed2173    
    Printed202    
    Emailed0    
    PDF Downloaded411    
    Comments [Add]    
    Cited by others 2    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]