Follicular growth and development under continuous gonadotropin-releasing hormone antagonist administration

Weissman, Ariel; Ravhon, Amir; Biran, G.; Levin, Daniel; Golan, Abraham; Levran, David

doi:10.1016/j.fertnstert.2007.01.119

Cited by 7 publications

(2 citation statements)

References 9 publications

(5 reference statements)

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“…Surprisingly, 2 patients in the LAP arm failed to suppress under continuous GnRH antagonist administration and developed a mature follicle that ruptured following hCG trigger, as previously described elsewhere [15]. This phenomenon has not been reported since, and may be related to a direct GnRH antagonist effect on the ovary.…”

Section: Discussionmentioning

confidence: 57%

Controlled Ovarian Stimulation Using a Long Gonadotropin-Releasing Hormone<b> </b>Antagonist Protocol: A Proof of Concept and Feasibility Study

Weissman

Ravhon²,

Steinfeld³

et al. 2013

Gynecol Obstet Invest

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Background/Aims: To evaluate the feasibility of a long protocol of controlled ovarian stimulation prior to in vitro fertilization (IVF) and embryo transfer with a gonadotropin-releasing hormone (GnRH) antagonist used for pituitary and ovarian suppression. Methods: Thirty patients undergoing IVF/intracytoplasmic sperm injection were randomized into two groups. The control group (n = 16) received a standard flexible GnRH antagonist protocol. Ovarian stimulation consisted of 225 IU/day of recombinant follicle-stimulating hormone for 5 days, followed by 225 IU/day of human menopausal gonadotropin until human chorionic gonadotropin (hCG) administration. The study group (n = 14) received 0.25 mg of GnRH antagonist daily for 7 days, thereafter, upon confirmation of pituitary and ovarian suppression, ovarian stimulation was commenced with the same protocol as used in the control group. Hormone and follicle dynamics, as well as laboratory characteristics and cycle outcome, were compared for both groups. Results: Both groups were comparable in baseline characteristics. Pituitary and ovarian suppression were effectively achieved in 12/14 patients in the study group. The duration of ovarian stimulation and gonadotropin consumption were similar in both groups, as was also the number and size of follicles on hCG day. Conclusion: The results of our study confirm the feasibility of a long GnRH antagonist protocol. This regimen could become another option to optimize GnRH antagonist protocols, and should thus be further explored.

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Section: Discussionmentioning

confidence: 57%

Controlled Ovarian Stimulation Using a Long Gonadotropin-Releasing Hormone<b> </b>Antagonist Protocol: A Proof of Concept and Feasibility Study

Weissman

Ravhon²,

Steinfeld³

et al. 2013

Gynecol Obstet Invest

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“…The ovary is one of the most dynamic endocrine organs, and follicular development can be classified into three phases according to their development stage and gonadotropin dependence: gonadotropin-independent phase, gonadotropin-responsive phase and gonadotropin-dependent phase [13] , [14] . The whole process includes follicle recruitment, selection, and ovulation.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Gonadotropin on Glucose Transport and Apoptosis in Rat Ovary

et al. 2012

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Although the effects of Gonadotropin on ovarian physiology have been known for many decades, its action on glucose uptake in the rat ovary remained poorly understood. Evidence also suggests that glucose uptake is mediated by a number of glucose transporter proteins (Glut). Therefore, we examined the rat ovary for the presence of Glut1–4 and blood glucose level after eCG (equine chorionic gonadotropin) and anti-eCG antiserum treatment. All of the glucose transports were present in the ovarian oocyte, granulosa cells and theca cells in different stage follicles. The expression of Glut in ovary was up-regulated by eCG, however, anti-eCG antiserum reversed eCG action. Western blot analysis also demonstrated the content of Glut1 was higher in eCG treatment group compared with anti-eCG antiserum and control group. The same tendency was shown in other glut isoforms. Moreover, there were no significant difference between the anti-eCG antiserum and control group. In additional, the level of serum glucose in eCG treatment group was significantly higher than others, which is similar with glut expression pattern. High glucose level in blood is correlated with increased expression of glucose transporter proteins in rat ovary. Meanwhile, anti-eCG antiserum increased granulosa cell apoptosis in antral follicle compared with those in eCG group. Our observations provide potential explanation for the effects of Glut on follicular development in rat ovary and a role for eCG in the regulation of ovarian glucose uptake.

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