Effects of Stilboestrol on Growth Hormone Secretion and Pituitary Cell Proliferation in the Male Rat

Lloyd, Helen; Meares, J. D.; Jacobi, Joan; Thomas, Frances J.

doi:10.1677/joe.0.0510473

Cited by 29 publications

(16 citation statements)

References 17 publications

(19 reference statements)

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“…Oestrogen may stimulate mitosis directly or may act indirectly through an intracellular effect mediated by the secretory activity which oestrogen induces (see " Discussion ", Lloyd et al, 1971). In the present experiment, the first mechanism, possibly acting on stem cells, may provide the means whereby the pituitary produces cells able to secrete prolactin.…”

Section: Table I Schedule Of Injections Of Diethylstilboestrol Dipropmentioning

confidence: 55%

“…Significant correlations were demonstrated previously between indices of GH secretion and mitotic activity during the early response to oestrogen (Lloyd et al, 1971). During the subsequent return to normal, an occasional gland showed raised mitotic as well as secretory activity several months after the dose (Lloyd et a/., 1972).…”

Section: Table I Schedule Of Injections Of Diethylstilboestrol Dipropmentioning

confidence: 66%

“…The initial response of the normal pituitary gland to oestrogen includes increased secretion of prolactin (Minaguchi et al, 1968;van der Gugten et al, 1970), adrenocorticotrophin (ACTH) (Gemzell, 1952) and growth hormone (GH) (Lloyd et al, 1971), the three hormones known to be secreted by tumours which eventually develop (Furth and Clifton, 1966). The early changes in GH secretion and mitotic activity over the course of the first 28 days after a single large dose of oestrogen have been described in some detail (Lloyd et al, 1971). The investigation now reported extended over a period of 70 days of repeated oestrogen administration and is based upon radioimrnunoassay of both prolactin and GH.…”

Section: Of Apparent Equilibrium In Mass Reached By the Pituitary Glamentioning

confidence: 99%

“…The procedures for radioimmunoassay of G H (Lloyd et al, 1971) and prolactin were based on the dextran-coated charcoal method (Lau et al, 1966) using reagents kindly provided by NIAMD through the Rat Pituitary Hormone Distribution Program. Results for G H are expressed in terms of NIAMD-Rat-GH-RP-I and for prolactin in terms of NIAMD-Rat-Prolactin-RP-1.…”

Section: Radioimmunoassaymentioning

confidence: 99%

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Secretory and mitotic response of the male rat pituitary gland to repeated doses of oestrogen

Lloyd

Meares

Jacobi

1973

Intl Journal of Cancer

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Section: Table I Schedule Of Injections Of Diethylstilboestrol Dipropmentioning

confidence: 55%

Section: Table I Schedule Of Injections Of Diethylstilboestrol Dipropmentioning

confidence: 66%

Section: Of Apparent Equilibrium In Mass Reached By the Pituitary Glamentioning

confidence: 99%

Section: Radioimmunoassaymentioning

confidence: 99%

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Secretory and mitotic response of the male rat pituitary gland to repeated doses of oestrogen

Lloyd

Meares

Jacobi

1973

Intl Journal of Cancer

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“…In addition, the combined administration of oestradiol and growth hormone (Table 1) produced no greater effects than those of each hormone alone, suggesting a common mechanism of action. Moreover, since oestrogen administration has been shown to increase plasma growth hormone levels (Frantz & Rabkin, 1965;Lloyd, Meares, Jacobi & Thomas, 1971), growth hormone may represent the pituitary 'feminizing factor' responsible for mediating the actions of oestradiol on hepatic steroid and drug metabolism.…”

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confidence: 99%

Feminization of Hepatic Steroid and Drug Metabolizing Enzymes by Growth Hormone in Male Rats

Krämer¹,

Colby²

1976

Journal of Endocrinology

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Many studies have established the importance of the gonadal hormones in the regulation of hepatic steroid and drug metabolism in rats (Yates, Herbst & Urquhart, 1958;Kitay, 1963;Conney, 1967; Gillette, Davies & Sasame, 1972). The activity of hepatic steroid \g=D\4-hydrogenase, the rate-limiting step in corticosteroid metabolism, is enhanced by oestradiol and diminished by testosterone administration. Consequently livers from female rats metabolize corticosteroids more rapidly than those from male rats. In contrast the metabolism of many drug substrates by hepatic microsomal cytochrome P-450-containing enzymes is increased by testosterone (Quinn, Axelrod & Brodie, 1958) and inhibited by oestradiol (Murphy & DuBois, 1958), resulting in a sex difference in oxidative drug metabolism opposite to that in reductive (\g=D\4-hydrogenase) steroid metabolism. We recently reported that the effects of gonadal hormone on both hepatic steroid and drug metabolism are manifested only in

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Role of somatostatin in the modulation of hypophysial growth hormone production by gonadal steroids

Gross

1980

Am. J. Anat.

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Growth hormone-release-inhibiting hormone (somatostatin) has been localized in several central nervous system sites, but the contribution of somatostatin in these various loci to the control of growth hormone (GH) production is unclear. In the present study, the efficacy of castration, alone, or with subsequent gonadal steroid administration, in modulating hypophysial GH production was examined, and the response of somatostatin-containing nerve endings in the median eminence and the organum vasculosum of the lamina terminalis (OVLT) was evaluated by means of immunocytochemistry. Orchidectomy reduced the size and number of immunoreactive GH-cells, and testosterone administration prevented this change. Ovariectomy appeared to stimulate the somatotropes, but this effect was neither as dramatic nor as consistent as the effect of castration in the male. Administration of estradiol, however, resulted in a marked reduction in the number, size, and GH content of somatotropes in all animals examined. Somatostatin was localized in the ext.erne1 lamina of the median eminence and in nerve endings surrounding the core of capillaries in the OVLT. Only the median eminence responded to steroid manipulations with a visible change in the immunoreactive pool of somatostatin, with a decrease following orchidectomy, which was reversible by testosterone treatment, and an increase following ovariectomy, which was reversible by estradiol treatment. However, as in the GH responses to steroid manipulations, the somatostatin responses were more variable in females than in males.These results suggest that: 1) testosterone promotes and estradiol, a t least at high doses, inhibits storage of GH in the anterior pituitary; 2 ) these changes in GH production may be regulated, in part, by altered somatostatin release from the median eminence into the hypophysial portal blood; and 3) somatostatin in the OVLT may not be involved in the steroid-induced modulation of GH production.Currently available evidence supports the hypothesis that a dual neural regulation of growth hormone (GH) secretion exists. The predominant control is believed to be stimulatory, mediated by a growth hormone-releasing factor (Martin, '76). Although the existence of this releasing factor is supported by considerable experimental evidence, its isolation and characterization have not been achieved; thus, specific techniques for its localization and measurement can not yet be applied. The inhibitory control is thought to be mediated by growth hormone-release-inhibiting hormone, or somatostatin, which has been isolated, char. acterized, and synthesized (Brazeau et al., '73). Using both radioimmunoassay (Brownstein e t al., '75; Epelbaum e t al., '77; Kobayashi et al., '77; Pate1 and Reichlin, '78) and immunocytochemistry (see Zimmerman, '77; Elde e t al., '78 for reviews), somatostatin has been localized in several central nervous system sites, including both hypothalamic and extrahypothalamic areas. There appear to be several general patterns of somatostatin localizatio...

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Effects of Stilboestrol on Growth Hormone Secretion and Pituitary Cell Proliferation in the Male Rat

Cited by 29 publications

References 17 publications

Secretory and mitotic response of the male rat pituitary gland to repeated doses of oestrogen

Secretory and mitotic response of the male rat pituitary gland to repeated doses of oestrogen

Feminization of Hepatic Steroid and Drug Metabolizing Enzymes by Growth Hormone in Male Rats

Role of somatostatin in the modulation of hypophysial growth hormone production by gonadal steroids

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