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The induction of ovulation and follicular luteinization in the guinea-pig by follicle-stimulating (FSH) and luteinizing (LH) hormones was studied in the intact and in the hypophysectomized animal. Follicular luteinization could be produced as early as day 8 of the oestrous cycle by 250 mu. FSH, but not before day 10 by 400 mu. LH, while either FSH or LH caused ovulation when given on day 12 or later. When injected on day 13, luteinization could be induced with 62·5 mu. FSH or 200 mu. LH. Luteinization of follicles also occurred when 400 mu. LH or 250 mu. FSH was given immediately after hypophysectomy on day 13, but when hormone treatment was delayed for 4·5 h after surgery the incidence of luteinization was greatly reduced. Combined treatment with 200 mu. LH and 125 mu. FSH, by contrast, readily caused luteinization. It is concluded that ovarian follicles are resistant to luteinization during the first half of the oestrous cycle and that the response to LH late in the cycle is dependent upon the maintenance of follicular responsiveness by endogenous gonadotrophin.

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Three experiments are described on the effects of oestrone and progesterone over wide dose ranges on the development of the mammary gland in the ovariectomized guinea-pig. Factorial designs were used so that the responses to both steroids could be studied simultaneously. The degree of mammary development was assessed by objective and by subjective methods.

The observation of previous workers that complete mammary development could be evoked in the guinea-pig by oestrogen alone was not confirmed. Over a wide dose range of oestrone better development of the gland was obtained if progesterone was also administered. On some dose levels of oestrone the synergistic effects of progesterone were very marked.

Maximal mammary development was observed with a daily dose of 10–50 μg oestrone in combination with 1000 μg progesterone. Considerable lobule-alveolar development was observed with progesterone alone when the daily dose was sufficiently high (2400 μg). No histological abnormalities were observed in the glands except in those developed on the lowest dose of oestrone to give significant growth effects (0·1 μg), in which there was some evidence of cystic changes.

The significance of the progesterone: oestrogen ratio in mammary development is discussed.

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D. J. Flint, R. A. Clegg and C. H. Knight


Prolactin implants prevented the decline in milk yield and the resumption of oestrous cycles which occurred between days 22 and 28 in untreated lactating rats. Ovariectomy and progesterone implants only partially prevented the decline in milk yield despite preventing the occurrence of oestrous cycles. All three treatments increased total RNA content of the mammary gland compared with controls. In untreated rats there were no changes in mammary DNA content or the number of insulin receptors whereas lipoprotein lipase (LPL) activity decreased significantly during the declining phase of lactation. In contrast, the number of insulin receptors, LPL activity and glucose incorporation into lipid increased in adipose tissue. Prolactin prevented the increase in insulin receptors and lipid synthesis and significantly decreased LPL activity in adipose tissue. Progesterone stimulated LPL activity in the mammary gland and also prevented the increase in lipid synthesis and insulin receptors in adipose tissue but was without effect on LPL activity whereas ovariectomy stimulated LPL activity in the mammary gland but prevented only the increase in the number of insulin receptors in adipose tissue.

The results show that raising the serum prolactin concentration can prevent the decline in milk yield during extended lactation and whilst part of this effect may be due to a direct effect on the mammary gland and an indirect effect due to inhibition of oestrous cycles, prolactin may also produce part of its effect on milk synthesis by inhibiting competitive metabolic processes in tissues such as adipose tissue.

J. Endocr. (1984) 102, 231–236

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K. J. Teerds, J. Closset, F. F. G. Rommerts, D. G. de Rooij, D. M. Stocco, B. Colenbrander, C. J. G. Wensing and G. Hennen


The effects of pure FSH and/or LH preparations on the number of Leydig cells and their function in immature hypophysectomized rats have been investigated. As a result of hypophysectomy at the age of 17–18 days, the number of recognizable Leydig cells per testis decreased, as did the steroidogenic capacity in vivo and in vitro. Treatment with 64 μg FSH on both 22 and 23 days of age, did not affect the number of recognizable Leydig cells. In contrast, two injections of LH (10 μg) caused a sixfold increase in the number of Leydig cells, but had a negative effect on spermatogenesis. These stimulatory and inhibitory effects of LH diminished when FSH was added. Treatment with FSH for 7 days caused a twofold increase in the number of Leydig cells when compared with hypophysectomized controls. 3β-Hydroxysteroid dehydrogenase (3β-HSD) and esterase activity in Leydig cells also increased under the influence of FSH. The pregnenolone production per Leydig cell in the presence of 5-cholesten-3β,22(R)-diol (22R-hydroxycholesterol) as substrate showed a sevenfold increase. Plasma testosterone levels 2 h after injection of human chorionic gonadotrophin in intact rats and hypophysectomized FSH-treated rats were the same. Following LH treatment for 7 days, the number of Leydig cells proved to be 11 times higher, and 3β-HSD and esterase activity were not different from intact controls. The testicular pregnenolone production was four- to fivefold higher when compared with untreated hypophysectomized rats. However, pregnenolone production per Leydig cell in LH-treated rats was only slightly different from the hypophysectomized controls.

In conclusion, FSH treatment caused an increase in the number and steroidogenic activity of Leydig cells, and LH had a major effect on the number of Leydig cells, but did not stimulate the steroidogenic capacity.

Journal of Endocrinology (1989) 120, 97–106

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MA Lawson, D Li, CA Glidewell-Kenney and FJ Lopez

Androgens have a profound effect on the hypothalamic-pituitary axis by reducing the synthesis and release of the pituitary gonadotropin LH. The effect on LH is partly a consequence of a direct, steroid-dependent action on pituitary function. Although androgen action has been well studied in vivo, in vitro cell models of androgen action on pituitary gonadotropes have been scarce. Recently, an LH-expressing cell line, LbetaT2, was generated by tumorigenesis targeted to the LH-producing cells of the mouse pituitary. The purpose of these studies was to determine the presence of androgen receptor (AR) and establish its function in this cell line. RT-PCR analysis indicated that the LbetaT2 cell line expresses AR mRNA. Transient transfection assays, using the mouse mammary tumor virus (MMTV) promoter, showed that a functional AR is also present. Testosterone (TEST), dihydrotestosterone (DHT), 7alpha-methyl-19-nortestosterone (MENT), and fluoxymesterone (FLUOXY) increased reporter gene activity in the rank order of potencies MENT>DHT> TEST>FLUOXY. Additionally, activation of MMTV promoter activity by DHT in LbetaT2 cells was diminished by the AR antagonists casodex and 2-hydroxy-flutamide, indicating that the effects of DHT are mediated through AR. In summary, these studies showed that the LbetaT2 cell line is a useful model for the evaluation and molecular characterization of androgen action in pituitary gonadotropes.

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Insulin, adrenal corticosteroid, and prolactin are minimal hormonal requirements for the development of secretion in cultures of pregnant mouse mammary gland (Rivera, 1964; Juergens, Stockdale, Topper & Elias, 1965). Augmentation of the rate of DNA synthesis is one of the hormone-initiated events associated with the developmental process, and this is primarily due to insulin (Juergens et al. 1965). Recently, human growth hormone (HGH) and human chorionic somatomammotrophin (HCS) have been shown to act similarly to prolactin in inducing functional changes in mammary organ cultures (Forsyth, 1967; Turkington, 1968a; Rivera, 1970). These hormones, having similar intrinsic prolactin-like activities, contain considerably more growth hormone activity than prolactin, and it was of interest to assess their growth-promoting activity in mammary gland cultures.

The growth hormone activity of the HGH (Upjohn lot no. 8717-DAD-100.3) was 2·5 units/mg. assayed by the 8-day 'body-weight gain' test against bovine growth hormone (NIH lot no. B-10). The HCS

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Department of Zoology, Iowa State University, Ames, Iowa 50010, U.S.A.

(Received 9 May 1977)

Griffith & Turner (1961) have shown that between day 20 of pregnancy and day 3 of lactation, the amount of DNA in rat mammary glands increases by 40%. To investigate hormonal regulation of this lactational growth phase, Griffith & Turner (1963) used an experimental model in vivo. They injected adult virgin ovariectomized rats with 2 μg oestradiol benzoate and 6 mg progesterone daily for 20 days to promote mammary growth equivalent to that of late pregnancy. During the next 3 days (days 21-23) the rats received daily injections of 2 mg prolactin, 1·5 mg growth hormone (GH), 250 μg cortisol acetate, or combinations of these hormones, in an attempt to induce a 'lactational-like' increase in mammary DNA. The rats were killed on day 24 and the DNA content of the six abdominal-inguinal glands was determined. Several

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S. G. Hillier

The gonadotrophins follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were first isolated in more or less pure forms over half a century ago. Purified pituitary gonadotrophins were used by Fevold (1941) and Greep, Van Dyke & Chow (1942) in their classic experiments which demonstrated unequivocally the need for both FSH and LH to stimulate normal ovarian follicular development and oestrogen secretion in hypophysectomized rats. Human pituitary gonadotrophins of equivalent purity have never been widely available for clinical use, but within the next few years pharmaceutical grades of human recombinant FSH and LH are both likely to become so (e.g. Keene, Matzuk, Otani et al. 1989). Taking account of recent advances in our understanding of gonadotrophin action at the cellular level, it should be possible to use these pure human gonadotrophins to devise improved strategies for stimulating ovarian function in infertile women.

Development-dependent follicular responsiveness to gonadotrophins

FSH receptors are located

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K Soumano, JG Lussier and CA Price

This study tested the hypothesis that luteal LH receptor (LHr) and follicular LHr and FSH receptor (FSHr) steady-state mRNA levels are greater during superovulation with equine chorionic gonadotrophin (eCG) compared with that with FSH. Heifers were stimulated with eCG (n = 10) or FSH (n = 10), and ovaries were recovered the day before and at 12 and 24 h after luteolysis was induced with prostaglandin F2 alpha (PGF2 alpha). Total RNA was purified from individual follicles and corpora lutea. Steady-state levels of LHr and FSHr mRNA were assessed by slot blot analysis employing homologous cDNA probes. There were no differences in luteal LHr between FSH- and eCG-stimulated animals before luteolysis, and hybridization signals were detected in only one of six animals by 12 h after injection of PGF2 alpha. After PGF2 alpha injection, steady-state levels of follicular LHr were 4-fold lower (P < 0.05) and follicular FSHr mRNA levels were 2.4-fold lower (P < 0.05) in eCG- compared with FSH-treated cattle. In eCG-treated animals, induction of luteolysis led to a significant increase in follicular LHr mRNA levels (P < 0.01) and a significant decrease in follicular FSHr mRNA levels (P < 0.01). There was no such effect of luteolysis in FSH-treated animals. We conclude that superovulation with eCG, compared with FSH, results in lower follicular levels of LHr and FSHr mRNA but does not affect luteal LHr mRNA levels.

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M Feldman, W Ruan, I Tappin, R Wieczorek and DL Kleinberg

Both GH and insulin-like growth factor I (IGF-I) synergize with estrogen to induce normal mammary gland development. However, the nature of this synergy has not been explored. To gain insight into the mechanism of these interactions we have examined the effects of these substances on the estrogen receptor (ER). ER levels in the mammary gland cytosols from hypophysectomized and oophorectomized rats, were measured using two assay systems: a dextran-coated charcoal procedure to measure binding to radiolabeled steroid, and an immunologic assay employing a specific antibody to the receptor. In both assays, levels of ER were at or near baseline detection (approximately 1-2 ng/mg protein). Treating animals with either bovine or human GH significantly increased ER activity (P<0.001), whereas prolactin (PRL) and/or estradiol treatment had no effect. That this increase was at the level of transcription was demonstrated by reverse transcriptase/polymerase chain reaction. Following a single injection of GH (50 microgram), a substantial increase in ER mRNA was observed by 10 h, with levels returning to baseline within 24 h; a concomitant increase in ER itself was also observed at the 10 h time point. The effect of GH appeared to occur mainly in the mammary stroma, because there were no differences in GH stimulation of ER between gland-free and gland containing mammary fat pads. Furthermore, analysis of mammary gland ER by immunocytochemistry demonstrated that while ER was present in the epithelial cells of non-treated animals, only GH treated animals had ER clearly visible in both glandular and fat cells of the tissue. In contrast, treating animals with des(1-3)-IGF-I did not result in reproducible increases in ER, nor in the staining of fat cell nuclei for ER. These data demonstrate a specific GH effect on the ER in the mammary fat cell.