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Heterologous radioimmunoassays for FSH and LH were employed to examine the effect of synthetic LH-RH upon gonadotrophin secretion in the ferret. Intravenous injection of 4 μg LH-RH induced a surge of FSH and of LH secretion in male and in female animals. In intact and in castrated males, the rise of LH was much more marked than that of FSH. The gonadotrophin response to LH-RH was greater in anoestrous than in oestrous females; FSH secretion was not enhanced during oestrus. Ovariectomized females behaved as anoestrous females with respect to LH secretion, while FSH secretion remained unchanged. Treatment of ovariectomized females with progesterone did not alter the pattern of response to LH-RH, but oestradiol treatment depressed the reaction to match that seen in oestrous females. Repetitive injections of LH-RH induced repetitive surges of FSH and LH in anoestrous females, but only of LH during oestrus: slow i.v. infusion of LH-RH induced a sustained elevation of plasma LH levels both in oestrous and in anoestrous females; again FSH levels rose only in anoestrous females. Injection of synthetic TRH did not alter gonadotrophin secretion in corresponding groups of male or female ferrets.

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Lisa M Arendt, Lindsay C Evans, Debra E Rugowski, Maria Jose Garcia-Barchino, Hallgeir Rui and Linda A Schuler

Epidemiologic studies have demonstrated that increased prolactin (PRL) exposure raises the risk of invasive estrogen receptor α (ERα)-positive breast cancer in women. However, the mechanism(s) whereby this occurs and the interactions with estrogen itself in this disease remain poorly understood. In order to investigate the role of ovarian hormones in the disease process, we employed a transgenic model neu-related lipocalin (NRL)–PRL in which transgenic PRL is directed to mammary epithelial cells by the PRL- and estrogen-insensitive NRL promoter, mimicking the endogenous PRL expression within the breast observed in women. This high local exposure leads to mammary lesion development and eventually carcinomas. Ovariectomy (ovx), shortly after puberty, did not alter the incidence or latency of PRL-induced mammary carcinomas, consistent with the independence of PRL from circulating estrogens as a risk factor for invasive breast cancer in women. However, chronic estrogen administration to ovx NRL–PRL females decreased the latency of both ERα-positive and -negative tumors. We identified multiple mechanisms that may underlie this observation. Elevated estrogen exposure cooperated with PRL to increase epithelial proliferation and myoepithelial abnormalities, increasing the incidence of preneoplastic lesions. Critical components of the extracellular matrix secreted by the myoepithelium were reduced with age, and transgenic PRL raised transcripts for tenascin-C and maspin, both associated with tumor progression and poor prognosis in subclasses of clinical breast tumors. Mammary pERK1/2 and pAkt, but not phosphorylated Stat5, were markedly elevated by local PRL. Together, these findings indicate that PRL employs multiple mechanisms to promote mammary tumorigenesis.

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In 1930 Fevold and Hisaw reported a separation of pituitary gonadotrophin into two fractions—a follicle-stimulating hormone (FSH) and a luteinizing hormone (LH). FSH when injected into immature or hypophysectomized rats caused follicular growth in the ovaries with no luteinization. LH injected by itself had no follicle-stimulating properties in such animals but would luteinize the follicles produced by FSH injection. Their separation [Fevold, Hisaw, and Leonard, 1931] depended on the greater solubility of FSH in cold distilled water. Evans, Meyer, and Simpson [1933] were unable to confirm these results, nor were Van Dyke and Wallen-Lawrence [1933].

In 1933 Fevold, Hisaw, Hellbaum, and Hertz published a method of separation by the selective adsorption of LH on benzoic acid. Saunders and Cole [1938] failed to confirm this, though they obtained some degree of separation.

In 1934 Wallen-Lawrence separated two fractions by precipitation with alcohol at 6° C. The precipitate with 40% alcohol was

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The effects of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) on plasma testosterone levels were examined in hypophysectomized and in intact immature and adult male rats. The animals were injected with saline, LH, FSH, or both gonadotrophins twice daily for 3·5 days and were killed 3 h after the last injection. Plasma testosterone levels were measured by radioimmunoassay.

In immature hypophysectomized rats, plasma testosterone levels were not changed by treatment with LH, FSH or LH plus FSH. The weight of the testes and of the seminal vesicles was increased only in animals injected with both LH and FSH.

In adult hypophysectomized rats, LH caused the expected increase in plasma testosterone levels, while FSH injected alone had no effect. Plasma testosterone levels in rats treated with 5 μg LH and 20 μg FSH were significantly greater than those in animals given 5 μg LH alone. However, the same dose of FSH did not potentiate the action of 25 μg LH on plasma testosterone levels. In adult hypophysectomized rats the weight of testes was not affected by any of the treatments. The weight of the seminal vesicles was increased by the higher dose of LH and addition of FSH caused no further increase.

In intact immature and adult rats plasma testosterone levels and the weight of testes were not changed by any of the treatments. Seminal vesicle weight was increased only in adult rats treated with the higher dose of LH together with FSH.

The results demonstrate that FSH potentiates the action of low doses of LH on plasma testosterone levels in adult hypophysectomized rats and suggest that FSH may be involved in the regulation of androgen secretion by the rat testis.

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W. J. de Greef, G. A. M. Eilers, J. de Koning, B. Karels and F. H. de Jong


Intraperitoneal administration of bovine follicular fluid (bFF) decreased plasma concentrations of FSH in ovariectomized rats after 2–3 h, while plasma LH and prolactin were unaffected. In untreated ovariectomized animals the concentrations of these hormones were found to show pulsatile variations. Concomitant occurrence of peak values of LH and FSH was found in about 40% of the pulses. No pulses of FSH were observed after i.p. treatment with bFF or partly purified preparations of inhibin from bFF, but the pulsatile release of LH and prolactin remained similar. Infusion of bFF into the lateral ventricle of the brain did not alter the concentrations of FSH, whereas administration of bFF into the pituitary gland diminished the plasma concentrations of FSH.

Anaesthesia (urethane plus xylazine) did not prevent the occurrence of the pulses of FSH and LH, but it reduced the pulse amplitude and clearance. During this anaesthesia, the concentrations of LHRH in the hypophysial stalk plasma decreased by 30% after administration of bFF, but did not alter after treatment with partly purified preparations of inhibin. It is concluded that the inhibin-like activity in bFF suppresses pulsatile FSH secretion in ovariectomized rats by an action on the pituitary gland, but has no effect on the pulsatile release of LH and prolactin.

J. Endocr. (1987) 113, 449–455

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M. Kobayashi, R. Nakano and A. Ooshima


Ovaries from 37 women with normal menstrual cycles were analysed for localization of pituitary gonadotrophins and gonadal steroids using an immunohistochemical method. In the follicular phase, FSH and oestradiol-17β localized in the granulosa layer, and LH, progesterone and testosterone localized in the internal thecal layer. In the luteal phase, gonadotrophins and steroids localized in luteal cells. Particularly in the early luteal phase, FSH and oestradiol-17β localized in large luteal cells, and LH, progesterone and testosterone localized in small luteal cells. The results of the present immunohistochemical analysis confirm the two-cell, two-gonadotrophin hypothesis of steroidogenesis in the human ovary.

Journal of Endocrinology (1990) 126, 483–488

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M R Sairam, A A H Zaky and A A Hassan


The isolation of highly purified forms of pituitary LH from Egyptian male (Nile) buffaloes is described. The total LH content (receptor binding activity) which was approximately 30 to 50 fold higher than FSH in the pituitary could be divided into three pools based upon fractionation patterns on a cation exchanger. The acidic fraction which also contained FSH was not purified to homogeneity. A basic fraction (bu-LH-2; 300 mg/kg anterior pituitary) and a very basic fraction (bu-LH-3; 80 mg/kg) were both highly purified and free of FSH activity as tested by specific FSH receptor and immunoassays. The basic buffalo LH fraction, bu-LH-2, was as active as highly purified ovine LH (oLH). The most basic form of buffalo LH, bu-LH-3, was, however, about twice as active as highly purified oLH in the in vitro bioassay using mouse Leydig tumour (MA-10) cells. In a receptor binding assay employing 125I-labelled buffalo LH (bu-LH-3) and porcine testicular membranes, the affinity of bu-LH-3 was about five times higher than purified oLH. The M r of both forms of purified buffalo LH and subunits was similar to that of oLH. Amino acid composition of buffalo LH was also very similar to oLH except for small differences. Fractionation by fast protein liquid chromatography on Mono-Q columns revealed further evidence of microheterogeneity in each of the pools of buffalo LH with bu-LH-3 exhibiting a predominant single component. By reverse-phase high-pressure liquid chromotography analysis we have localized differences in the two purified isoforms of male buffalo LH to the α subunit. It is suggested that differences in biological potencies could be due to variations in terminal glycosylation and/or differences in branching of this subunit which is known to be important for signal transduction.

Journal of Endocrinology (1994) 143, 313–323

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K. Taya and S. Sasamoto


To determine whether failure of follicular maturation during the early stages of lactation in rats is due to inadequate LH stimulation, lactating rats nursing eight pups were injected twice daily for 1–3 days (days 2–5 of lactation) with various doses of ovine LH. Follicular maturation was determined by the ability of the follicles to ovulate in response to 10 IU human chorionic gonadotrophin (hCG), endogenous oestradiol-17β and inhibin production. Ovulation was not induced in control animals in response to 10 IU hCG given between days 2 and 5 of lactation. On the other hand, an injection of 10 IU hCG could induce ovulation in LH-treated animals, in which 25 and 50 μg LH per injection were given s.c. from days 2 to 5 of lactation. Concentrations of oestradiol-17β and inhibin activity in ovarian venous plasma increased progressively after the administration of LH, indicating that induced development of ovulatory follicles had occurred. Plasma concentrations of FSH declined in LH-treated animals compared with those in control animals. The decrease in plasma concentrations of FSH was not observed when lactating rats were ovariectomized before the first injection of LH, indicating that ovarian products, probably inhibin, from developing follicles may suppress the secretion of FSH from the pituitary gland. In both LH-treated and control animals, concentrations of prolactin and progesterone remained increased during the period of LH administration. The present results, therefore, suggest that the plasma levels of LH are an important determinant of follicular maturation during lactation in rats.

J. Endocr. (1988) 116, 115–122

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Plasma FSH concentrations in rats have been determined by radioimmunoassay under a variety of experimental conditions to see whether any evidence could be obtained of an acute divergence in LH and FSH secretion rates which would support the idea of separate, specific hypothalamic releasing factors for these two hormones.

During the normal ovarian cycle and after the administration of progesterone to female rats on the morning of the day of pro-oestrus increased secretion of both LH and FSH began simultaneously but FSH concentrations were later maintained or increased slightly while LH concentrations were falling. During early pregnancy FSH concentrations were higher than at the corresponding stage of the cycle at a time when LH concentrations had been shown to be lower. Progesterone injected at the dioestrous stage of the cycle reduced both LH and FSH concentrations though the effect on LH was more marked. After ovariectomy at any stage of the oestrous cycle or on day 4 of pregnancy there was a rapid and significant increase in plasma FSH concentration which was quite different from the delayed increase in LH concentration observed in these animals. In contrast, the early increase in FSH concentration in male rats after castration was less than the increase in LH concentration. The final FSH concentration in castrated males was only about four times the basal level in contrast to the 10- to 15-fold increase in LH in males and both LH and FSH in females. Anovulatory adult females that had received 1·25 mg of testosterone propionate on day 4 of postnatal life showed the rapid and sustained increase in plasma FSH after ovariectomy that was seen in normal females.

None of these results strongly support the idea that separate and specific hypothalamic releasing factors for LH or FSH are secreted in the rat although the differences in the early response to gonadectomy could be explained on this basis.

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C. G. Tsonis, A. S. McNeilly and D. T. Baird


The secretion of oestradiol and inhibin were measured during the follicular and luteal phase of the cycle by a sensitive bioassay using sheep pituitary cells in culture in four ewes in which the left ovary had been autotransplanted to the neck. On day 12 of the cycle, premature luteal regression was induced with an injection of 100 μg cloprostenol (prostaglandin F analogue; PG) and ovarian venous blood was collected every 4 h for 72 h. These same four ewes were infused in the ensuing cycle with NIH-oFSH-S14 at 10 μg/h for 48 h immediately after an injection of PG and sampled as above.

During the luteal phase ( − 2 h before PG) both in the control and FSH-infused cycles the inhibin secretion rate (SR) was 27–45 units/min. After PG injection, the inhibin SR declined with time to reach 3·6–5 units/min at the onset of the LH surge (60 h after PG) in the control cycle. In contrast, in the following cycle infusion of FSH after PG injection caused a slight increase in the inhibin SR which then remained raised at 42–50 units/min for up to 60 h after PG. In the late follicular phase the oestradiol SR was greater in the FSH-infused than in the control cycles, indicating multiple follicular development. In the FSH-infused cycle the preovulatory surges of LH and FSH were markedly attenuated.

These data demonstrate that (1) inhibin SR is high during the luteal phase suggesting that the sheep corpus luteum secretes inhibin, (2) in the control cycle inhibin SR declines during follicular maturation at a time when oestradiol SR is increasing but FSH levels are decreasing, and (3) exogenously administered FSH stimulates the secretion of inhibin from the ovary during the follicular phase.

J. Endocr. (1988) 117, 283–291