The effect of ovariectomy on gonadotropin release

Yen, S. S. C.; Tsai, C. C.

doi:10.1172/jci106587

Cited by 64 publications

(22 citation statements)

References 17 publications

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“…Recent studies from our laboratory have indicated that the feedback effect of estradiol on gonadotropin release exhibited a biphasic response (initial suppression followed by augmentation) and a differential effect on the release of LH and FSH exists. Quantitatively, estradiol exerts more inhibitory action on FSH release and more augmented release on LH (12,(22)(23)(24). Taken together these data support the hypothesis that the pattern of LH-FSH release during the human menstrual cycle can be accounted for by the negative and positive feedback systems involving ovarian estrogen.…”

Section: Discussionsupporting

confidence: 65%

Acute Gonadotropin Release Induced by Exogenous Estradiol During the Mid-Follicular Phase of the Menstrual Cycle

Yen

Tsai

1972

The Journal of Clinical Endocrinology & Metabolism

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115

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During the mid-follicular phase of the cycle (D7-9), a rapid increase in serum estradiol levels was induced via 17P-estradiol infusion, ethinyl estradiol and estradiol benzoate administration in a fashion simulating the preovulatory rise and this elicited an acute release of LH to a lesser degree FSH, in 5 of 7 subjects studied. During treatment (1-3 days) a uniform suppression of gonadotropin levels was noted. This negative feedback effect was followed by the onset of an acute surge of both gonadotropins which occurred 12-24 hrs after the termination of treatment when a consistent drop of serum estradiol concentrations was observed. In three subjects the induced LH-FSH surge was comparable to those occurring spontaneously at midcycle, but without evidence of ovarian response either in ovulation or in the enhanced estradiol secretion.In all subjects, this transient disruption of the normal sequence of gonadotropin secretion was associated with an impairment of follicular maturation as reflected by the low estradiol levels and the prolongation of the follicular phase. The subsequent time course mimicked a newly initiated cycle with an inversed relationship between serum estradiol and gonadotropin concentrations. These data suggest that the negative and positive feedback action of ovarian estradiol modulates the tonic secretion of gonadotropins during the human menstrual cycle and supports the hypothesis that the rapid rise (or acute fall) in serum estradiol levels during the late follicular phase provides a major ovarian signal for triggering the gonadotropin surge at midcycle. (/ Clin Endocr 34: 298, 1972) C OMPELLING evidence that increasing levels of circulating estradiol trigger the ovulatory surge of LH is afforded by the ability of exogenous estradiol to induce acute release of LH in rats (1,2), sheep (3,4), and monkeys (5). Additionally, administration of antibodies to 17|3-estradiol blocks spontaneous and PMS-induced LH surges in rats which can be restored by treatment with a non cross-reacting synthetic estrogen, diethylstilbesterol (6,7). In humans, although ovulation and a rise in plasma LH may be induced by administration of estrogen in

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Section: Discussionsupporting

confidence: 65%

Acute Gonadotropin Release Induced by Exogenous Estradiol During the Mid-Follicular Phase of the Menstrual Cycle

Yen

Tsai

1972

The Journal of Clinical Endocrinology & Metabolism

Self Cite

115

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“…We have not been able to find a previous reference to this possibilitv. There are several lines of evidence supporting the presence of an inhibin. First, during menopause, FSH and LH appear to change proportionally when estrogen is given (22)(23)(24), and the two appear to rise proportionately after castration (25)(26). A similar proportional fall in gonadotropins was noted with the spontaneous rise in E2 during the two anovulatory cycles of Fig.…”

Section: Resultsmentioning

confidence: 88%

Hormonal characteristics of the human menstrual cycle throughout reproductive life.

Sherman¹,

Korenman²

1975

J. Clin. Invest.

530

158

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A B S T R A C T The changes in serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol, and progesterone that occur both early and late in reproductive life were characterized and compared with findings in young, normal women and in patients with certain menstrual disorders.A total of 50 complete menstrual cycles in 37 women were examined. Five distinct patterns of hormonal regulation were found, three of which are reported here: (a) A long follicular phase and delayed follicular maturation in young women with long, unpredictable intermenstrual intervals from menarche; (b) a short follicular phase with increasing age and in short cycles in perimenopausal women; and (c) true anovulatory vaginal bleeding in long cycles in perimenopausal women.The short cycles before and during the menopausal transition were found to have lower E2 levels and high FSH concentrations throughout, while LH remained in the normal range. During long cycles in perimenopausal women, concentrations of LH and FSH were in the menopausal range. However, follicular maturation was observed months after high levels of gonadotropins were attained.These studies permit the characterization of the menstrual history of the normal woman in terms of the hormonal changes that occur and provide a basis for the definition of several disorders of follicular maturation.

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“…However, although the effect of E2 on pituitary gonadotropin secre tion is biphasic [27], administration of E2 (during the E2 test) after complete pituitary desensitization by GnRH-A only reduced the levels of serum LH and FSH still further, this effect being more pronounced for FSH than for LH. An analogous effect has been demonstrated in GnRH-pretreated rats [28] in which E2 administration provoked a decline in serum LH and FSH levels, whereas it stimulated release in untreated controls.…”

Section: Discussionmentioning

confidence: 91%

Induction of Pharmacological Hypogonadotropism Using Gonadotropin-Releasing Hormone Agonists in Patients Undergoing Controlled Ovarian Stimulation

Lindner

Braendle

Lichtenberg

et al. 1990

Gynecol Obstet Invest

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Pharmacological hypogonadotropism was induced in 167 women using the gonadotropin-releasing hormone agonists (GnRH-A) buserelin acetate or triptorelin acetate. 84 patients (group 1) began treatment using 1.2 mg/ day buserelin acetate intranasally during the follicular phase (days 1–3); 41 patients (group II) began the same treatment, supported by 10 mg medroxyprogesterone acetate for 10 days, during the early luteal phase; 42 patients (group 3) received triptorelin acetate as an intramuscular depot injection, supported by 10 mg medroxyprogesterone acetate for 10 days, during the early luteal phase. Serum luteinizing hormone, follicle-stimulating hormone, oestradiol (E₂), prolactin, and testosterone levels were monitored. Pituitary function was assessed by (1) measurement of endogenous luteinizing hormone fluctuation; (2) response to luteinizing hormone releasing hormone administration, and (3) response to oestradiol benzoate (E₂ test). Complete pituitary desensitization was only assumed, if all three tests were negative. The LH-RH test and the E₂ test were shown to be the most reliable indicator of pituitary function. E₂ administration led to further reduction of gonadotropin secretion after pituitary desensitization. The desensitization time was 41.1 ± 11.7 days in group 1 and was significantly reduced to 20.7 ± 10.5 days in group 2 (p < 0.01); a further, non-significant shortening to 15.1 ± 3.0 days was observed in group 3. Changes in endocrine parameters demonstrated hypogonadotropic hypo-oestrogenism after initial pituitary stimulation.

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The effect of ovariectomy on gonadotropin release

Cited by 64 publications

References 17 publications

Acute Gonadotropin Release Induced by Exogenous Estradiol During the Mid-Follicular Phase of the Menstrual Cycle

Acute Gonadotropin Release Induced by Exogenous Estradiol During the Mid-Follicular Phase of the Menstrual Cycle

Hormonal characteristics of the human menstrual cycle throughout reproductive life.

Induction of Pharmacological Hypogonadotropism Using Gonadotropin-Releasing Hormone Agonists in Patients Undergoing Controlled Ovarian Stimulation

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