A Biphasic Model for the Hormonal Control of Testicular Descent

Hutson, J. M.

doi:10.1016/s0140-6736(85)92739-4

Cited by 204 publications

(117 citation statements)

References 13 publications

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“…The fetal testis secretes three hormones essential for normal masculinization; anti-Mullerian hormone (AMH), which causes degeneration of the Mullerian (paramesonephric) ducts, androgens, which act to stabilize the Wolffian (mesonephric) ducts and to masculinize the external genitalia, and insulin-like 3 (INSL3), which acts with testosterone to induce testicular descent (Hutson 1985, Nef & Parada 1999, Zimmermann et al 1999, Klonisch et al 2004. Expression of AMH is stimulated by direct action of SOX9 and steroidogenic factor 1 (NR5A1; Morais et al 1996, de Santa et al 1998, Arango et al 1999, and the Sertoli cells start to secrete AMH very quickly after initial differentiation (12.5 dpc in the mouse and 8.5 GW in the human) to ensure timely regression of the female duct precursors (Picon 1969, Munsterberg & Lovell-Badge 1991, Rajpert-De Meyts et al 1999.…”

Section: Fetal Testicular Hormone Productionmentioning

confidence: 99%

Endocrinology of the mammalian fetal testis

O’Shaughnessy¹,

Fowler²

2011

Reproduction

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The testes are essential endocrine regulators of fetal masculinization and male development and are, themselves, subject to hormonal regulation during gestation. This review focuses, primarily, on this latter control of testicular function. Data available suggest that, in most mammalian species, the testis goes through a period of independent function before the fetal hypothalamic-pituitary-gonadal axis develops at around 50% of gestation. This pituitary-independent phase coincides with the most critical period of fetal masculinization. Thereafter, the fetal testes appear to become pituitary hormone-dependent, concurrent with declining Leydig cell function, but increasing Sertoli cell numbers. The two orders of mammals most commonly used for these types of studies (rodents and primates) appear to represent special cases within this general hypothesis. In terms of testicular function, rodents are born 'early' before the pituitary-dependent phase of fetal development, while the primate testis is dependent upon placental gonadotropin released during the pituitary-independent phase of development.

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Section: Fetal Testicular Hormone Productionmentioning

confidence: 99%

Endocrinology of the mammalian fetal testis

O’Shaughnessy¹,

Fowler²

2011

Reproduction

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“…Testicular descent is thought to be a biphasic process: there is an initial migration from a position near the lower pole of the kidney down to the lower abdomen, followed by a second phase through the inguinal canal to the scrotum (3). This relative transabdominal movement of the testis is believed to result from both the degeneration of the cranial suspensory ligament (CSL) and the development of the gubernaculum which are respectively attached to the cranial and caudal aspects of the testis (1).…”

Section: Introductionmentioning

confidence: 99%

“…This relative transabdominal movement of the testis is believed to result from both the degeneration of the cranial suspensory ligament (CSL) and the development of the gubernaculum which are respectively attached to the cranial and caudal aspects of the testis (1). CSL degeneration is an androgen dependent process as androgen receptor (AR) deficient male mice have failure of the CSL to regress, along with maldescended testes (3,4).…”

Section: Introductionmentioning

confidence: 99%

Genetic analysis of the INSL3 gene in patients with maldescent of the testis

et al. 2001

European Journal of Endocrinology

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Objective: Testicular maldescent is important because it is a common congenital disorder that is associated with an increased risk of infertility and testicular cancer. Murine studies indicate that testicular maldescent can result from disruption of insulin-like factor 3 (INSL3) activity and that it may be more severe when there is concurrent undermasculinisation. Therefore, the INSL3 gene was screened for mutations and polymorphisms that may contribute to testicular maldescent in patients with undermasculinisation as well as those with isolated testicular maldescent. Methods and Results: The patient groups consisted of individuals with isolated testicular maldescent n 28 and patients with undermasculinised genitalia and intra-abdominal n 24 or inguinal gonads n 33X The three control groups were: normal males n 15Y males with undermasculinised genitalia and scrotal gonads n 29 and females n 82X SSCP/HA mutation screening detected eight variants, five of which were predicted to alter the protein sequence (A-1G, V19L, P25S, A36T, R78H). Three of the amino acid changes (A-1G, V19L, R78H) each occurred in a single control sample and one was identified in a male with undermasculinised genitalia and intraabdominal testes (P25S). The A36T amino acid polymorphism was found in both patient and control groups at a similar frequency. Conclusions: The evidence suggests that INSL3 mutations and polymorphisms are not a major cause of testicular maldescent with or without associated undermasculinisation.

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“…It is generally agreed that testicular descent in mammals occurs in two distinct steps with different anatomy and hormonal regulation (Hutson, 1985;Amann and Veeramachaneni, 2007;Foresta et al, 2008;Hughes and Acerini, 2008;Feng et al, 2009). In the first, or transabdominal phase, the genitoinguinal ligament, also known as the ''gubernaculum,'' undergoes enlargement or the ''swelling reaction.''…”

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Development of the Gubernaculum During Testicular Descent in the Rat

Nation

Buraundi

Farmer

et al. 2011

The Anatomical Record

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Gubernacular elongation during inguinoscrotal testicular descent and cremaster muscle development remains poorly described in mammals. The role of the genitofemoral nerve (GFN) remains elusive. We performed detailed histological analysis of testicular descent in normal rats to provide a comprehensive anatomical description for molecular studies. Fetuses and neonatal male offspring (5-10 per group) from time-mated Sprague-Dawley dams (embryonic days 15, 16, and 19; postnatal days 0, 2, and 8) were prepared for histology. Immunohistochemistry was performed for nerves (Class III tubulin, Tuj1) and muscle (desmin). At embryonic days 15 and 16, the gubernaculum and breast bud are adjacent and both supplied by the GFN. By embryonic day 19, the breast bud has regressed and the gubernacular swelling reaction is completed. Postnatally, the gubernacular core regresses, except for a cranial proliferative zone. The cremaster is continuous with internal oblique and transversus abdominis. By postnatal day 2 (P2), the gubernaculum has everted, locating the proliferative zone caudally and the residual mesenchymal core externally. Eversion creates the processus vaginalis, with the everted gubernaculum loose in subcutaneous tissue but still remote from the scrotum. By P8, the gubernaculum has nearly reached the scrotum with fibrous connections attaching the gubernaculum to the scrotal skin. A direct link between GFN, gubernaculum, and breast bud suggests that the latter may be involved in gubernacular development. Second, the cremaster muscle is continuous with abdominal wall muscles, but most of its growth occurs in the distal gubernacular tip. Finally, gubernacular eversion at birth brings the cranial proliferative zone to the external distal tip, enabling gubernacular elongation similar to a limb bud. Anat Rec, 294:1249Rec, 294: -1260Rec, 294: , 2011. V V C 2011 Wiley-Liss, Inc.

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A Biphasic Model for the Hormonal Control of Testicular Descent

Cited by 204 publications

References 13 publications

Endocrinology of the mammalian fetal testis

Endocrinology of the mammalian fetal testis

Genetic analysis of the INSL3 gene in patients with maldescent of the testis

Development of the Gubernaculum During Testicular Descent in the Rat

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