Exogenous oestrogens prevent transabdominal testicular descent in mice with complete androgen resistance (testicular feminisation)

1987 ◽  
Vol 2 (4) ◽  
Author(s):  
JohnM. Hutson
Keyword(s):  
Testicular Descent ◽  
Androgen Resistance ◽  
Testicular Feminisation

Hormonal control of testicular descent and the cause of cryptorchidism

1994 ◽  
Vol 6 (2) ◽  
pp. 151 ◽  
Author(s):  
JM Hutson ◽  
M Baker ◽  
M Terada ◽  
B Zhou ◽  
G Paxton
Keyword(s):  
Undescended Testis ◽  
Good Evidence ◽  
Hormonal Control ◽  
Testicular Descent ◽  
Second Phase ◽  
Rodent Models ◽  
Paper Briefly ◽  
Calcitonin Gene ◽  
Androgen Resistance ◽  
Androgen Levels

This paper briefly reviews the literature on testicular descent and presents new observations from the authors' laboratory which suggest new ways of looking at old problems. There is now good evidence that testicular descent occurs in two morphologically and hormonally distinct phases. Relative 'transabdominal migration' of the testis compared with the ovary occurs at 10-15 weeks of gestation in the human and 'inguinoscrotal' migration occurs at 26-35 weeks of gestation. We have proposed previously that the first phase is controlled by Mullerian inhibiting substance although this remains controversial. The second phase is androgen dependent and is possibly mediated indirectly through the release from the genitofemoral nerve (GFN) of the neuropeptide calcitonin gene-related peptide (CGRP). Recently we have used three different rodent models of undescended testis to determine the involvement of the GNF and/or CGRP. The testicular feminization mouse with complete androgen resistance and the rat exposed prenatally to the antiandrogen flutamide have a deficiency of CGRP in the GFN. In contrast, the mutant trans-scrotal rat which has normal androgen levels has an excess of CGRP in the GFN. All cryptorchidism models, despite their different primary cause, have in common an abnormality of the GNF and/or CGRP which is consistent with the hypothesis that normal testicular descent in the rodent may be mediated by the GFN.

Exogenous androgens reduce the expression of INSL3, a hormone involved in normal testicular descent, in fetal Leydig cells

2014 ◽  
Author(s):  
W Colin Duncan ◽  
Fiona Connolly ◽  
Lyndsey Boswell ◽  
Graeme Burt ◽  
Alan S McNeilly ◽  
...  
Keyword(s):  
Leydig Cells ◽  
Testicular Descent ◽  
Fetal Leydig Cells

The Gubernaculum and the Evolution of Testicular Descent

HAPS Educator ◽  
2017 ◽  
Vol 21 (3) ◽  
pp. 12-19 ◽  
Author(s):  
David M. Darda
Keyword(s):  
Testicular Descent

scholarly journals INSL3/LGR8 role in testicular descent and cryptorchidism

2005 ◽  
Vol 10 (1) ◽  
pp. 49-54 ◽  
Author(s):  
NV Bogatcheva ◽  
AI Agoulnik
Keyword(s):  
Testicular Descent

Analysis of the CAG tract length in the Androgen Receptor gene in Mexican patients with nonsyndromic cryptorchidism

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Daniel A. Landero-Huerta ◽  
Rosa M. Vigueras-Villaseñor ◽  
Lucía Taja-Chayeb ◽  
Fabiola García-Andrade ◽  
Elena Aréchaga-Ocampo ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Germ Cell ◽  
Receptor Gene ◽  
Germ Cell Tumors ◽  
Androgen Receptor Gene ◽  
Testicular Descent ◽  
Healthy Individuals ◽  
Testicular Germ Cell ◽  
Molecular Alteration ◽  
Mexican Patients

Abstract Objectives Cryptorchidism is the most common genitourinary birth defect in live newborn males and is considered as an important risk factor for testicular germ cell tumors and infertility. The Androgen Receptor gene is important in this pathology due to its participation, mainly, in the inguinoscrotal phase of testicular descent. We determine the length of the CAG tract in the Androgen Receptor (AR) gene in Mexican patients with nonsyndromic cryptorchidism. Methods One hundred and 15 males were included; of these, 62 had nonsyndromic cryptorchidism and 53 were healthy volunteers. DNA was extracted from a peripheral blood samples, subsequently, the CAG tract in exon 1 of AR gene was amplified by PCR and sequenced. Results Mexican patients with nonsyndromic cryptorchidism presented 25.03 ± 2.58 repeats of CAG tract in the AR gene compared to 22.72 ± 3.17 repeats of CAG tract in Mexican healthy individuals (p≤0.0001; t value of 4.3). Furthermore, the deletion of codon 57 that corresponds to the deletion of a leucine residue at position 57 (Del L57) in the AR gene was found for the first time in a nonsyndromic cryptorchidism patient. This molecular alteration has been related previously to testicular germ cell tumor (TGCT). Conclusions The CAG tract in the AR gene is longer in patients with nonsyndromic cryptorchidism than in healthy individuals, supporting the association between this polymorphism of the AR gene and nonsyndromic cryptorchidism in the Mexican population.

Association of antimullerian hormone with the size of the appendix testis, the androgen and estrogen receptors and their expression in the appendix testis, in congenital cryptorchidism

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Xenophon Sinopidis ◽  
Eirini Kostopoulou ◽  
Andrea Paola Rojas-Gil ◽  
Antonios Panagidis ◽  
Eleni Kourea ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Receptor Expression ◽  
Testicular Descent ◽  
Antimullerian Hormone ◽  
Mullerian Ducts ◽  
Score Method ◽  
Antimüllerian Hormone ◽  
Unilateral Cryptorchidism ◽  
Appendix Testis

Abstract Objectives Antimullerian hormone (AMH) causes regression of the mullerian ducts in the male fetus. The appendix testis (AT) is a vestigial remnant of mullerian duct origin, containing both androgen (AR) and estrogen (ER) receptors. The role of both AMH and AT in testicular descent is yet to be studied. We investigated the possible association of AMH with AT size, the AR and ER, and their expression in the AT, in congenital cryptorchidism. Methods A total of 26 patients with congenital unilateral cryptorchidism and 26 controls with orthotopic testes were investigated, and 21 ATs were identified in each group. AMH and insulin-like three hormone (INSL3) concentrations were measured with spectrophotometry. AR and ER receptor expression was assessed with immunohistochemistry using monoclonal antibodies R441 for AR and MAB463 for ER. For the estimation of receptor expression, the Allred Score method was used. Results AMH concentrations did not present significant differences between patients with congenital cryptorchidism and the controls. Also, no correlation was found between AMH, INSL3, and AT length. Allred scores did not present significant differences. However, expression percentiles and intensity for both receptors presented significant differences. Three children with cryptorchidism and the highest AMH levels also had the highest estrogen receptor scores in the AT. Conclusions No association was found between AMH and the studied major parameters. However, higher AMH concentrations, in combination with higher estrogen receptor scores in the AT, may play a role in cryptorchidism in some children. Larger population samples are needed to verify this observation.

Normative Values for Testicular Descent from Infancy to Adulthood

1993 ◽  
Vol 39 (3-4) ◽  
pp. 118-121 ◽  
Author(s):  
J. Sack ◽  
B. Reichman ◽  
A. Fix
Keyword(s):  
Normative Values ◽  
Testicular Descent
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