Gonadotrophin-releasing hormone treatment for induction of follicular maturation and ovulation in amenorrhoeic women with anorexia nervosa.

Nillius, Sven Johan; Wide, Leif

doi:10.1136/bmj.3.5980.405

Cited by 54 publications

(5 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The lack of understanding of the precise nature of GnRH control on gonado¬ trophin secretion may hinder the clinical use of this decapeptide and may ex¬ plain its present low success rates, for example in the treatment of anovulatory patients (Zanartu et al 1974;Zarate et al 1976;Nillius & Wide 1975;Schneider et al 1977;Breckwoldt et al 1974;Keller 1973). In vivo studies on the control of LH and FSH secretion by GnRH have primarily included experiments on the effects of single or multiple injections (Krey et al 1973;Ferin et al 1974;Hoff et al 1977;Wang et al 1976;Joffe & Keye 1975).…”

mentioning

confidence: 99%

PITUITARY AND OVARIAN HORMONAL RESPONSE TO 48 h GONADOTROPHIN RELEASING HORRMONE (GnRH) INFUSIONS IN FEMALE RHESUS MONKEYS

Ferin

Bogumil

Drewes

et al. 1978

Acta Endocrinologica

View full text Add to dashboard Cite

The effects of prolonged gonadotrophin-releasing hormone (GnRH) infusions on LH, FSH, oestrogens and progesterone secretion were studied in female rhesus monkeys at various times of the menstrual cycle and after castration. GnRH was infused at the rate of 15 \g=m\g/h for 48 h. This resulted in mean peripheral GnRH levels of 398 \m=+-\ 31.5 pg/ml (\m=+-\se) as measured by radioimmunoassay. As expected the pattern of gonadotrophin responses to GnRH varied considerably with the phase of the menstrual cycle. The largest LH increase was seen during the late follicular phase (6-fold over baseline), with a 3-fold increase during the luteal phase and a 2-fold one during the early follicular phase and in the period following the LH surge. Significant FSH increases (4-fold) were seen only during the follicular phase. Oestrogens increased about 2-fold within 4 h of the start of the infusion during the early follicular phase. In the late follicular phase and during the LH surge, they declined within 24 and 1 h, respectively. Large progesterone increases were seen only during the luteal phase. Of special interest is the fact that the increase in gonadotrophin secretion could not be maintained for the entire duration of the experiment even though GnRH continued to be infused at rates sufficient to elicit initial increases of several fold over baseline. Gonadotrophin release declined 4\p=n-\28 h after the initial stimulation. A further decrease below pre-infusion

show abstract

mentioning

confidence: 99%

PITUITARY AND OVARIAN HORMONAL RESPONSE TO 48 h GONADOTROPHIN RELEASING HORRMONE (GnRH) INFUSIONS IN FEMALE RHESUS MONKEYS

Ferin

Bogumil

Drewes

et al. 1978

Acta Endocrinologica

View full text Add to dashboard Cite

show abstract

“…Ovarian sex steroid production is essential for follicular growth and subsequent ovulation in nearly every animal (25)(26)(27). In frogs and fish, these steroids also appear to be critical regulators of oocyte maturation (28,29), which is defined as the resumption of meiosis from prophase I to metaphase II.…”

Section: Discussionmentioning

confidence: 99%

Xenopus laevis Ovarian CYP17 Is a Highly Potent Enzyme Expressed Exclusively in Oocytes

Yang

Lutz

Hammes

2003

Journal of Biological Chemistry

View full text Add to dashboard Cite

Progesterone has long been considered the primary mediator of Xenopus oocyte maturation. We have recently shown, however, that androgens, which are equal or more potent promoters of maturation and are present at higher levels in ovulating frogs, may also be playing an important physiologic role in mediating maturation. Here, we examined the role of CYP17, a key enzyme mediating sex steroid synthesis, in Xenopus ovarian androgen production. We found that the 17,20-lyase activities of Xenopus CYP17 exceeded the 17␣-hydroxylase activities in both the ⌬4 and ⌬5 pathways; thus, Xenopus CYP17 rapidly converted pregnenolone and progesterone to dehydroepiandrosterone (DHEA) and androstenedione, respectively. This remarkably robust activity exceeds that of CYP17 from most higher vertebrates, and likely explains why virtually no progesterone is detected in ovulating frogs. Additionally, ovarian CYP17 activity was present exclusively in oocytes, although all other enzymes involved in sex steroid production were expressed almost entirely in surrounding follicular cells. This compartmentalization suggests a "two-cell" model whereby Xenopus ovarian androgen production requires both follicular cells and oocytes themselves. The requirement of oocytes for ovarian androgen production further introduces the unusual paradigm whereby germ cells may be responsible for producing important steroids used to mediate their own maturation.The phenomenon of steroid-induced maturation of Xenopus oocytes has served as a model for studying cell cycle and nongenomic steroid signaling for several decades (1-5). During this time, progesterone has been considered the primary physiologic mediator of oocyte maturation, perhaps through interactions with classical progesterone receptors expressed in the oocyte (6, 7). We have recently shown, however, that testosterone, rather than progesterone, may be the primary physiologic mediator of Xenopus oocyte maturation (8). This dominant role of testosterone is evidenced by the observation that testosterone is a substantially more potent activator of oocyte maturation than progesterone, and that testosterone levels are significantly higher than progesterone (which is nearly undetectable) in the serum and ovaries of ␤-HCG 1 -stimulated frogs. In addition, we have shown that, in vitro, isolated oocytes rapidly convert exogenously added progesterone to the androgen androstenedione (AD), which is an equally potent promoter of maturation when compared with progesterone. These data suggest that both AD and progesterone are likely inducing maturation under in vitro conditions typical for "progesteronemediated" maturation.The high levels of ovarian testosterone in the absence of detectable progesterone imply that Xenopus ovaries are extremely efficient at metabolizing progesterone. Additionally, the ability of isolated oocytes to rapidly convert progesterone to androgens suggests that the oocytes themselves may be important contributors to progesterone metabolism in the ovary. To explain the lack of in vivo progeste...

show abstract

“…The synthetic gonadotrophin releasing hormone (LHRH) can be used to restore LH and FSH pulsatility in patients with hypogonadotrophic hypogonadism (HH), with hypothalamic (Crowley & McArthur, 1980) or organic pituitary disease (Mason et al, 1984) or with functional disorders such as anorexia nervosa (Nillius & Wide, 1975). Long-term Correspondence: H. S. Jacobs.…”

Section: Discussionmentioning

confidence: 99%

Gonadotrophin Control of Follicular Development

Abdulwahid

Adams

Spuy

et al. 1985

Clinical Endocrinology

View full text Add to dashboard Cite

In order to investigate the endocrine requirements for induction of follicle maturation, ovulation and luteal function we have measured plasma LH and FSH concentrations in 109 cycles induced by treatment with LHRH in 25 women with amenorrhoea of diverse aetiology. The major clinical and endocrine subgroupings were polycystic ovarian disease (PCO), Kallmann's syndrome, weight related amenorrhoea and hyperprolactinaemia. By analysis of variance of the LH and FSH concentrations obtained three times per week in the follicular phase in 77 ovulatory cycles (including 24 conception cycles), we found that in women with PCO the mean LH concentration was 19.5 IU/l. In hyperprolactinaemia and secondary amenorrhoea of non-specific aetiology the mean LH concentration was 11.6 IU/l and in patients with hypogonadotrophic hypogonadism and weight-related amenorrhoea it was 7.2IU/l. These mean LH concentrations were significantly different from each other (P less than 0.001). We speculate that the high LH concentrations in the follicular phase may impair the final stages of oocyte maturation and so contribute to the infertility of these patients. FSH concentrations in the follicular phase were lower in patients with hypogonadotrophic hypogonadism and weight-related amenorrhoea than in other groups. Although the differences were statistically significant (P less than 0.001) the difference was small (mean FSH in hypogonadotrophic hypogonadism and weight-related amenorrhoea 4.3 IU/l vs 6.3 IU/l in the others) and of uncertain biological significance. During the luteal phase, no differences between any of the groups in LH and FSH concentrations were found.

show abstract

Gonadotrophin-releasing hormone treatment for induction of follicular maturation and ovulation in amenorrhoeic women with anorexia nervosa.

Cited by 54 publications

References 6 publications

PITUITARY AND OVARIAN HORMONAL RESPONSE TO 48 h GONADOTROPHIN RELEASING HORRMONE (GnRH) INFUSIONS IN FEMALE RHESUS MONKEYS

PITUITARY AND OVARIAN HORMONAL RESPONSE TO 48 h GONADOTROPHIN RELEASING HORRMONE (GnRH) INFUSIONS IN FEMALE RHESUS MONKEYS

Xenopus laevis Ovarian CYP17 Is a Highly Potent Enzyme Expressed Exclusively in Oocytes

Gonadotrophin Control of Follicular Development

Contact Info

Product

Resources

About