Skip Navigation


Human Reproduction Update Advance Access originally published online on May 3, 2006
Human Reproduction Update 2006 12(5):557-571; doi:10.1093/humupd/dml020
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
12/5/557    most recent
dml020v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (18)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Messinis, I. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Messinis, I. E.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Ovarian feedback, mechanism of action and possible clinical implications

Ioannis E. Messinis

Department of Obstetrics and Gynaecology, University of Thessalia, Medical School, 22 Papakiriazi Street, 41222 Larissa, Greece

To whom correspondence should be addressed at: Department of Obstetrics and Gynaecology, University of Thessalia, Medical School, 22 Papakiriazi Street, 41222 Larissa, Greece. E-mail: messinis{at}med.uth.gr

The secretion of gonadotrophins from the pituitary in women is under ovarian control via negative and positive feedback mechanisms. Steroidal and non-steroidal substances mediate the ovarian effects on the hypothalamic-pituitary system. During the follicular phase of the cycle, estradiol (E2) plays a key role, while circulating progesterone (at low concentrations) and inhibin B contribute to the control of LH and FSH secretion respectively. During the luteal phase, both E2 and progesterone regulate secretion of the two gonadotrophins, while inhibin A plays a role in FSH secretion. The intercycle rise of FSH is related to changes in the levels of the steroidal and non-steroidal substances during the luteal-follicular transition. In terms of the positive feedback mechanism, E2 is the main component sensitizing the pituitary to GnRH. Activity of a non-steroidal ovarian substance, named gonadotrophin surge-attenuating factor (GnSAF), has been detected after ovarian stimulation. It is hypothesized that GnSAF, by antagonizing the sensitizing effect of E2 on the pituitary, regulates the amplitude of the endogenous LH surge at midcycle. Disturbances in the feedback mechanisms can occur in various abnormal conditions or after treatment with pharmaceutical compounds that interfere with the production or the action of endogenous hormones.

Key words: FSH / LH / estrogen / ovarian feedback / progesterone


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Biol. Reprod.Home page
V. Michopoulos, S. L. Berga, J. R. Kaplan, and M. E. Wilson
Social Subordination and Polymorphisms in the Gene Encoding the Serotonin Transporter Enhance Estradiol Inhibition of Luteinizing Hormone Secretion in Female Rhesus Monkeys
Biol Reprod, December 1, 2009; 81(6): 1154 - 1163.
[Abstract] [Full Text] [PDF]


Home page
Hum ReprodHome page
A. Gordon, R. Aguilar, J. C. Garrido-Gracia, S. Guil-Luna, R. Sanchez-Cespedes, Y. Millan, J. Martin de las Mulas, and J. E. Sanchez-Criado
Activation of estrogen receptor-{alpha} induces gonadotroph progesterone receptor expression and action differently in young and middle-aged ovariectomized rats
Hum. Reprod., October 1, 2009; 24(10): 2618 - 2628.
[Abstract] [Full Text] [PDF]


Home page
Mol. Endocrinol.Home page
P. Lamba, J. Fortin, S. Tran, Y. Wang, and D. J. Bernard
A Novel Role for the Forkhead Transcription Factor FOXL2 in Activin A-Regulated Follicle-Stimulating Hormone {beta} Subunit Transcription
Mol. Endocrinol., July 1, 2009; 23(7): 1001 - 1013.
[Abstract] [Full Text] [PDF]


Home page
ReproductionHome page
A. Gordon, J. C Garrido-Gracia, R. Aguilar, S. Guil-Luna, Y. Millan, J. M. de las Mulas, and J. E Sanchez-Criado
Ovarian stimulation with FSH reduces phosphorylation of gonadotrope progesterone receptor and LH secretion in the rat
Reproduction, January 1, 2009; 137(1): 151 - 159.
[Abstract] [Full Text] [PDF]


Home page
Toxicol PatholHome page
G. F. Weinbauer, M. Niehoff, M. Niehaus, S. Srivastav, A. Fuchs, E. Van Esch, and J. M. Cline
Physiology and Endocrinology of the Ovarian Cycle in Macaques
Toxicol Pathol, December 1, 2008; 36(7_suppl): 7S - 23S.
[Abstract] [Full Text] [PDF]


Home page
Toxicol PatholHome page
E. Buse, M. Zoller, and E. Van Esch
The Macaque Ovary, with Special Reference to the Cynomolgus Macaque (Macaca fascicularis)
Toxicol Pathol, December 1, 2008; 36(7_suppl): 24S - 66S.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
C. Andreu-Vieyra, R. Chen, and M. M. Matzuk
Effects of Granulosa Cell-Specific Deletion of Rb in Inha-{alpha} Null Female Mice
Endocrinology, August 1, 2007; 148(8): 3837 - 3849.
[Abstract] [Full Text] [PDF]


Home page
Hum ReprodHome page
H.M. Fatemi, C. Bourgain, P. Donoso, C. Blockeel, E.G. Papanikolaou, B. Popovic-Todorovic, and P. Devroey
Effect of oral administration of dydrogestrone versus vaginal administration of natural micronized progesterone on the secretory transformation of endometrium and luteal endocrine profile in patients with premature ovarian failure: a proof of concept
Hum. Reprod., May 1, 2007; 22(5): 1260 - 1263.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.