| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Journal of Andrology, Vol 13, Issue 6 534-542, Copyright © 1992 by The American Society of Andrology
JOURNAL ARTICLE |
P. van der Schoot and W. Elger
Department of Endocrinology and Reproduction, Faculty of Medicine and Health Sciences, Erasmus University--Rotterdam, The Netherlands.
Normal and disturbed testicular descent is frequently approached exclusively through a consideration of the caudal testicular suspensory apparatus. This is surprising, because embryonal gonads develop with both cranial and caudal suspensory ligaments, and the sexes differ with respect to the persistence and development of both the cranial and the caudal ligaments. The current study examined the possible role of fetal testicular androgens in male-specific failure of the development of the cranial gonadal suspensory apparatus in rats. Normal male fetuses were studied, as well as fetuses exposed to the anti-androgen flutamide from day 10 after conception. Females were given daily injections of methyl-testosterone alone or in combination with the anti-androgen cyproterone acetate from day 15 after conception, and were studied on day 22. The cranial ligaments remained of minor extension in normal males but developed considerably in females. They developed in female fashion in males exposed to flutamide, and persisted throughout postnatal life. Cranial ligaments did not develop in females that had been exposed to methyl-testosterone. Simultaneous treatment with a large dose of cyproterone acetate effectively counteracted this effect. Fetal testicular testosterone thus appears to play a key role in the prevention of the outgrowth of the cranial gonadal/genital ligament in rats. The supposed function of this suspensory apparatus makes it likely that its persistence in males, as the consequence of inappropriate androgen action during fetal life, facilitates disturbance of testicular descent. This finding may contribute to understanding developmental disorders underlying disturbed testis descent in humans.
This article has been cited by other articles:
![]() |
T. E. Willnow, A. Hammes, and S. Eaton Lipoproteins and their receptors in embryonic development: more than cholesterol clearance Development, September 15, 2007; 134(18): 3239 - 3249. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. P. Gorlov, A. Kamat, N. V. Bogatcheva, E. Jones, D. J. Lamb, A. Truong, C. E. Bishop, K. McElreavey, and A. I. Agoulnik Mutations of the GREAT gene cause cryptorchidism Hum. Mol. Genet., September 15, 2002; 11(19): 2309 - 2318. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Zimmermann, G. Steding, J. M. A. Emmen, A. O. Brinkmann, K. Nayernia, A. F. Holstein, W. Engel, and I. M. Adham Targeted Disruption of the Insl3 Gene Causes Bilateral Cryptorchidism Mol. Endocrinol., May 1, 1999; 13(5): 681 - 691. [Abstract] [Full Text] |
||||
![]() |
J. M. Hutson, S. Hasthorpe, and C. F. Heyns Anatomical and Functional Aspects of Testicular Descent and Cryptorchidism Endocr. Rev., April 1, 1997; 18(2): 259 - 280. [Abstract] [Full Text] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |