Studies on the mechanism of the selective suppression of plasma levels of follicle-stimulating hormone in the female rat after administration of steroid-free bovine follicular fluid

Greef, W. J. De; Jong, Frank H. de; Koning, Jan de; Steenbergen, Jacobie; Vaart, P. D. M. van der

doi:10.1677/joe.0.0970327

Cited by 23 publications

(25 citation statements)

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“…A larger difference was found in the circulatory T Y of rat FSH between the earlier findings on pituitary (40·5 min; de Greef et al 1983) and recFSH (88·4 min). The reason for the difference is not apparent, since pituitary FSH and recFSH should be structurally closer, due to the fact that the carbohydrates of FSH are not sulfated in the same way as those of LH.…”

Section: Discussioncontrasting

confidence: 72%

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Recombinant forms of rat and human luteinizing hormone and follicle-stimulating hormone; comparison of functions in vitro and in vivo

Hakola

Haavisto²,

Pierroz³

et al. 1998

Journal of Endocrinology

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We have previously described the preparation, purification and partial characterization of recombinant (rec) forms of rat luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In the present study, the special functional features of these hormones were studied further, in vitro and in vivo, and compared with human recLH and recFSH, as well as with human urinary choriongonadotropin (hCG) and rat pituitary LH (NIDDK-RP3). In radioreceptor assay, the affinity of hCG binding to rat testis membranes was 5-fold higher than that of human recLH and 100-fold higher than that of rat recLH. In in vitro bioassay, using dispersed adult mouse interstitial cells or a mouse Leydig tumor cell line (BLT-1), hCG and human recLH were 10-to 20-fold more potent than rat recLH. Correspondingly, rat pituitary LH was about 10-fold less potent than rat recLH, and evoked a maximum testosterone response that was about half of that elicited by the other LH/CG preparations. Rat recFSH was about 10-fold less potent than human recFSH in stimulating cAMP production of a mouse Sertoli cell line (MSC-1) expressing the recombinant rat FSH receptor.The circulating half-times (T Y ) of rat and human rec hormones were assessed after i.v. injections into adult male rats rendered gonadotropin-deficient by treatment with a gonadotropin-releasing hormone antagonist. A novel immunometric assay was used for the rat FSH measurements. In the one-component model the T Y values of rat and human recLH were 18·2 1·9 min (n=7) and 44·6 3·1 min (n=7) respectively and those of rat and human recFSH were 88·4 10·7 min (n=6) and 55·0 4·2 min (n=6) respectively; the two-component models revealed similar differences between the rec hormone preparations. Collectively, rat recLH was eliminated significantly faster from the circulation than human recLH (P<0·0001). In contrast, the elimination of rat recFSH was significantly slower than that of human recFSH (P=0·02).In conclusion, rat recFSH and rat recLH display lower biopotencies per unit mass than the respective human hormones in vitro, and also in vivo for LH. This is paralleled by shorter T Y of rat recLH than the respective human hormone in the circulation, whereas human recFSH has a shorter T Y than human FSH. The special functional features of the rat rec gonadotropins emphasize the use of these preparations on studies of gonadotropin function in the rat, an important animal model for reproductive physiology.

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Section: Discussioncontrasting

confidence: 72%

“…De Greef et al (1983) have reported previously a half-time of 18·6 min for rat LH after injection of adenohypophysial extracts in female rats. These data on LH are surprisingly similar to the T Y values measured for rat recLH in our study (18·2 min).…”

Section: Discussionmentioning

confidence: 95%

Recombinant forms of rat and human luteinizing hormone and follicle-stimulating hormone; comparison of functions in vitro and in vivo

Hakola

Haavisto²,

Pierroz³

et al. 1998

Journal of Endocrinology

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“…This has been proven true for the pituitary gland, since intact hemi-pituitaries exhibit a greater hormonal responsiveness than dispersed pituitary cells (Milenkovic et al 1989). Despite early studies suggesting a hypothalamic site of inhibin action (Lumpkin et al 1981, Condon et al 1983, Greef et al 1983, we and others (Gonzalez-Manchion et al 1991, Knight 1996 have been unable to find any effect of inhibin on basal GnRH release. This finding may support the hypothesis that the main site of inhibin action is the pituitary (Tilbrook et al 1993).…”

Section: Discussionmentioning

confidence: 78%

“…In addition to a pituitary site of action, effects of activins and inhibins on the release and/or biosynthesis of hypothalamic GnRH release have been suggested (Lumpkin et al 1981, Condon et al 1983, Greef et al 1983. The recent demonstration that -subunits and the activin receptor ActRII mRNA are present in hypothalamic regions involved in the release of GnRH provided the neuroanatomical basis for a possible effect of activins on GnRH release and/or biosynthesis , Cameron et al 1994.…”

Section: Discussionmentioning

confidence: 99%

Activin-A stimulates hypothalamic gonadotropin-releasing hormone release by the explanted male rat hypothalamus: interaction with inhibin and androgens

Calogero

Burrello²,

Ossino³

et al. 1998

Journal of Endocrinology

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The presence of activins in those hypothalamic regions containing gonadotropin-releasing hormone (GnRH)-secreting neurons suggests that these peptides may regulate the reproductive function modulating not only pituitary FSH release and biosynthesis, but also hypothalamic GnRH release. The purpose of this study was to evaluate the effects of activin-A, a homodimer of inhibin A subunit, on hypothalamic GnRH release in vitro and, because of their well known antithetical effects, to evaluate its interaction with inhibin. In addition, since androgens modulate the release of GnRH from male rat hypothalami, we thought it of interest to study the possible interplay between these steroids and activin on GnRH release. To accomplish this, we employed a hypothalamic organ culture system which enabled us to evaluate GnRH release from individually incubated hemi-hypothalami explanted from male rats. Activin-A stimulated GnRH release in a biphasic manner. The maximal effect was reached at a concentration of 10 ng/ml which increased GnRH output by about 75%. Inhibin abolished the stimulatory effect of a maximally effective concentration of activin-A in a dose-dependent manner, whereas alone it had no effect on GnRH output. As previously shown, testosterone (1 nmol/l) and dihydrotestosterone (DHT, 0·1 nmol/l) suppressed basal GnRH release, but only testosterone was able to inhibit the release of GnRH stimulated by activin-A. Since DHT is a non-aromatizable androgen, we evaluated whether the inhibitory effect of testosterone was due to its in vitro conversion into 17 -estradiol. The addition of 4-hydroxyandrostenedione, a steroidal aromatase inhibitor, did not influence the suppressive effect of testosterone on GnRH release stimulated by activin-A.In conclusion, activin-A stimulated hypothalamic GnRH release in vitro and this effect was abolished by inhibin and was blunted by testosterone. These findings suggest that activins may participate in the regulation of the hypothalamic-pituitary-gonadal axis by modulating GnRH release. The ability of testosterone to suppress the release of GnRH stimulated by activin-A indicates that this steroid has a potent negative feedback influence on GnRH release.

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“…Nevertheless, thirty-two rats per group as a minimum for measuring serum T is a much larger number than is commonly appreciated as necessary. For LH, Nett's approximation of a twenty-four-minute half-life is the higher end of the range of reported values, from thirteen to nineteen to twenty-three minutes (de Greef et al 1983;Weick 1977); in the following example, twenty minutes will be used as a representative number. Ellis and Desjardins (1982) give the range of interpulse intervals for LH as being from thirty-five to 360 minutes, with a mean of ninety-eight minutes.…”

Section: Measuring T and Lhmentioning

confidence: 99%

Assessment of Circulating Hormones in Regulatory Toxicity Studies II. Male Reproductive Hormones

Chapin

Creasy²

2012

Toxicol Pathol

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When test article-related testicular toxicity or Leydig cell tumors are identified in nonclinical studies, the measurement of circulating hormones such as luteinizing hormone, follicle-stimulating hormone, inhibin, testosterone, or prolactin is often considered in order to aid mechanistic investigations or to identify potential biomarkers in man. Although some hormone levels are relatively constant, others are subject to wide variability owing to pulsatility of secretion, diurnal rhythms, and stress. To avoid being misled, it is important that this variation is factored into any study design that includes hormone measurements. Since all these possibilities start from the pathologist's reading of the tissue sections, we begin with a review of the morphologic changes that are tied to underlying alterations in hormones. We then provide the reader with basic information and representative hormone data, including coefficients of variation, for the major male reproductive hormones in the three main nonclinical species (rats, dogs, and cynomolgus monkeys). Power and probability tables for rats and dogs allow estimates of the number of animals or samples needed to provide a given likelihood of detecting a hormonal change of a given size. More importantly, we highlight the variability of this process and the real value in readers developing this information at their own site.

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Studies on the mechanism of the selective suppression of plasma levels of follicle-stimulating hormone in the female rat after administration of steroid-free bovine follicular fluid

Cited by 23 publications

References 0 publications

Recombinant forms of rat and human luteinizing hormone and follicle-stimulating hormone; comparison of functions in vitro and in vivo

Recombinant forms of rat and human luteinizing hormone and follicle-stimulating hormone; comparison of functions in vitro and in vivo

Activin-A stimulates hypothalamic gonadotropin-releasing hormone release by the explanted male rat hypothalamus: interaction with inhibin and androgens

Assessment of Circulating Hormones in Regulatory Toxicity Studies II. Male Reproductive Hormones

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