The Effect of Altered Thyroid State on Prolactin Binding to Liver and 7,12-Dimethylbenz(a)anthracene-Induced Mammary Tumors in Rats

Smith, R. D.; Hilf, Russell; Senior, Alan E.

doi:10.3181/00379727-158-40237

Cited by 10 publications

(11 citation statements)

References 6 publications

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“…The present results confirm previous reports of the presence of specific binding sites for lactogenic hormones in the rat mammary gland (Kelly, Bradley, Shiu, Meites «fe Friesen, 1974;Reddy & Watkins, 1975;Holcomb et al 1976;Smith, Hilf «fe Senior, 1976;Bohnet, Gomez & Friesen, 1977). In this study prolactin binding was usually measured in a micro¬ somal fraction.…”

Section: Discussionsupporting

confidence: 92%

Ontogeny and Control of Prolactin Receptors in the Mammary Gland and Liver of Virgin, Pregnant and Lactating Rats

Hayden¹,

Bonney²,

Forsyth³

1979

Journal of Endocrinology

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Prolactin receptors were identified and partially characterized in the mammary gland of the rat. The binding of 125I-labelled ovine prolactin to a subcellular particulate fraction of rat mammary gland decreased between days 30 and 100 of age. Over the same period, binding to the liver increased and there was a significant negative correlation between prolactin binding in the two tissues. Binding to the mammary gland was low during pregnancy, increased in early lactation and declined after the litters were weaned. Binding to the liver was lower during lactation than during pregnancy or the period after weaning suggesting that tissue-specific factors may operate in the control of this receptor. In virgin rats, prolactin binding by the mammary gland was increased by oestrogen. This effect was blocked by hypophysectomy and partially restored by replacement therapy with prolactin. Hypothyroidism and treatment with progesterone also reduced the response to oestrogen. The maintenance of prolactin binding by the mammary gland of lactating rats depends on the presence of the ovaries and pituitary, thyroid and adrenal glands. Examination of the ratio epithelium: stroma suggests that prolactin acts by increasing the number of epithelial cells in the mammary gland and that thyroid, adrenal and ovarian hormones modulate the number of receptors per cell.

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Section: Discussionsupporting

confidence: 92%

Ontogeny and Control of Prolactin Receptors in the Mammary Gland and Liver of Virgin, Pregnant and Lactating Rats

Hayden¹,

Bonney²,

Forsyth³

1979

Journal of Endocrinology

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“…It was found that this receptor was present in much higher concentrations in female than male rats. These findings have been confirmed by other groups including our own (71)(72)(73)(74). The development of these receptors has been shown to follow that of the steroid-metabolizing enzymes rather closely.…”

Section: Central Control Of Prolactin (Pri) Receptors In the Liversupporting

confidence: 81%

Role of the Hypothalamo-Pituitary-Liver Axis in Sex Differences in Susceptibility of the Liver to Toxic Agents

Gustafsson¹,

Eneroth²,

Hökfelt³

et al. 1981

Environmental Health Perspectives

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At birth testicular androgens irreversibly program brain centers involved in hypothalamopituitary control of hepatic sex-dependent steroid and drug metabolism. This imprinting process results in activation of a hypothalamic "feminostatin"-a secreting center that is turned on just before puberty. Feminostatin inhibits pituitary secretion of "feminizing factor," a pituitary hormone that feminizes the basal type of metabolism characterizing the liver of hypophysectomized and gonadectomized rats. Consequently, female rats that are devoid of feminostatin will secrete feminizing factor from the pituitary, leading to a feminine type of hepatic metabolism. Male rats have an active feminostatin-secreting center, and inhibition of pituitary feminizing factor release results in an autonomous type of liver metabolism. Female rats show a relative androgen unresponsiveness and seem incapable of releasing feminostatin after treatment with natural androgens, possibly because of more efficient metabolism (breakdown) of androgen in the female than in the male rat brain.Frontal deafferentation at the retrochiasmatic and suprachiasmatic level resulted in a complete "feminization" of hepatic steroid metabolism in male rats. Such an effect was also seen when lesions involving mainly the anterior periventricular hypothalamic area and the suprachiasmatic nucleus were performed in male rats. No effects were seen in analogous lesions in female rats in any of the cases studied. These findings suggest that a region including the anterior hypothalamic periventricular area, the suprachiasmatic nucleus and adjacent areas is involved in the control of hepatic steroid metabolism. It is postulated that the neuronal cell bodies that produce feminostatin have their origins in this area of the hypothalamus or may send axons through this area to the basal hypothalamus and thus directly or indirectly influence the anterior pituitary gland.Regulation by the central nervous system of a "lactogenic" (prolactin, Prl) receptor, present in the female rat liver, was also studied. This receptor is present in very low concentration or absent in the male rat. Anterior hypothalamic deafferentation at the retrochiasmatic level in male rats increased the hepatic Prl receptor concentration to the female level 3-4 days following the operation. A transection rostral to the suprachiasmatic nucleus had no effect on the concentration of Prl receptors in male animals. Our results demonstrate that the number of Prl receptors is regulated by the hypothalamo-pituitary system. The receptor-inducing pituitary factor might be related to the feminizing factor. Experiments were carried out to elucidate the nature of the Prl receptor-inducing pituitary factor. April 1981 129Human growth hormone (hGH) continuously administered was shown to induce Prl receptors in livers from male and female hypophysectomized-gonadectomized rats. The prolactin receptors were increased to a level found in control female rat livers. This inductive effect of hGH was also seen in adrenalectomized and...

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“…Some previous studies (Costlow et al, 1976;Holdaway and Friesen, 1976;Kelly et al, 1974) suggested that changes in the growth of DMBA-induced mammary tumors following endocrine treatment may be reflected by changes in PRL binding to tumor cells. However, our study and others (DeSombre et al, 1976;Smith et al, 1976) …”

Section: Analysis Of Datacontrasting

confidence: 68%

“…These results may indicate regional heterogeneity of PRL receptors as previously reported (Smith et al, 1976) and a potential role of PRL in liver function which might affect mammary tumors through some growth factors (Francis and Hill, 1975) or enzyme modification (Richards, 1975). Some previous studies (Costlow et al, 1976;Holdaway and Friesen, 1976;Kelly et al, 1974) suggested that changes in the growth of DMBA-induced mammary tumors following endocrine treatment may be reflected by changes in PRL binding to tumor cells.…”

Section: Analysis Of Datasupporting

confidence: 67%

“…The response of a hormone-dependent tumor is likely to depend not only on the circulating hormone levels but also on hormone receptor levels. Specific receptors for estrogen (DeSombre et al, 1976;Leung and Sasaki, 1975;McGuire and Julian, 1971;Terenius, 1973), progesterone (Asselin et al, 1976;Horwitz and McGuire, 1977;Terenius, 1973) and PRL (Holdaway and Friesen, 1976;Smith et al, 1976) have been demonstrated in DMBA-induced mammary tumors. Furthermore, it has been reported that estrogen receptor levels in DMBA-induced rat mammary tumors are increased by estrogen and PRL (Asselin et al, 1977;Sasaki and Leung, 1975;Vignon and Rochefort, 1976), whereas PRL receptor levels are differently influenced by estrogen and PRL (Asselin et al, 1977;Holdaway and Friesen, 1976;Smith et al, 1976).…”

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confidence: 99%

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Effects of bromocriptine and tamoxifen on growth and hormone receptor levels of 7,12-dimethylbenz(a)anthracene-induced mammary tumors in rats.

et al. 1983

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The role of prolactin (PRL) and estrogen in the growth of 7,12-dimethylbenz(a)-anthracene (DMBA)-induced rat mammary tumors was investigated.Tumor growth was suppressed by both bromocriptine and tamoxifen.Combined administration of ovine PRL and tamoxifen attenuated the inhibitory action of tamoxifen on tumor growth. Serum PRL levels were decreased by both bromocriptine and tamoxifen administration.Estrogen receptors (ER) in tumor tissues were decreased in number by tamoxifen, but not by bromocriptine.Progesterone receptors (PgR) in DMBAinduced mammary tumors were abolished by tamoxifen and significantly reduced by bromocriptine.Combined administration of ovine PRL with tamoxifen attenuated the inhibition of PgR induced by tamoxifen alone, while ER remained undetectable. Specific PRL binding to the liver was significantly reduced by treatment with bromocriptine, tamoxifen and tamoxifen plus ovine PRL, whereas PRL receptors in mammary tumor were not influenced by these drugs.These results suggest that PRL may stimulate DMBA-induced tumor growth independently of ER and that a part of the inhibiting effect of tamoxifen on tumor growth may be explained by the decreased PRL secretion.

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The Effect of Altered Thyroid State on Prolactin Binding to Liver and 7,12-Dimethylbenz(a)anthracene-Induced Mammary Tumors in Rats

Cited by 10 publications

References 6 publications

Ontogeny and Control of Prolactin Receptors in the Mammary Gland and Liver of Virgin, Pregnant and Lactating Rats

Ontogeny and Control of Prolactin Receptors in the Mammary Gland and Liver of Virgin, Pregnant and Lactating Rats

Role of the Hypothalamo-Pituitary-Liver Axis in Sex Differences in Susceptibility of the Liver to Toxic Agents

Effects of bromocriptine and tamoxifen on growth and hormone receptor levels of 7,12-dimethylbenz(a)anthracene-induced mammary tumors in rats.

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