The inhibitory effect of progesterone on lactogenesis during pregnancy is already evident by mid- to late gestation in rodents (original) (raw)
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Suckling-induced prolactin release potentiates mifepristone-induced lactogenesis in pregnant rats
Reproduction, 1989
were not increased by suckling, but casein and lactose concentrations in the mammary gland showed values similar to those obtained in the mifepristonetreated non-suckling rats. Mifepristone can therefore potentiate suckling-induced prolactin release in pregnant rats, demonstrating a direct central inhibitory action of progesterone on prolactin secretion. This suckling-induced prolactin secretion, unable to induce casein or lactose synthesis in the presence of progesterone, enhanced significantly synthesis of these milk components in the absence of progesterone action (rats treated with mifepristone). Fatty acid synthase, which is stimulated by the suckling stimulus in lactating rats, was not modified by mifepristone or suckling in pregnant rats.
Journal of Endocrinology, 1991
The part played by the adrenergic system on the release of prolactin and lactogenesis induced by prostaglandin F2α and the antiprogesterone RU 486 was studied in pregnant rats. Two doses of prostaglandin F2α (150 μg) administered at 08.00 and 12.00 h on day 19 of pregnancy induced, at 12.00 h on day 20 (24 h after administration), a significant increase in the serum concentration of prolactin, with a significant decrease in serum progesterone levels. These hormonal changes significantly augmented casein and lactose levels in the mammary gland. Treatment with RU 486 (2 mg/kg) at 08.00 h on day 19 augmented casein and lactose concentrations in the mammary gland at 12.00 h on day 20 without modifying serum concentrations of prolactin and progesterone. The adrenergic antagonists, propranolol (3 mg/kg), metoprolol (10 mg/kg), ICI 118 551 (200 μg/kg), idazoxan (100 μg/kg) and prazosin (10 mg/kg), were administered s.c. at 12.00 and 20.00 h on day 19 and 08.00 h on day 20 of pregnancy to i...
Effects of prolactin withdrawal on activity of pyruvate dehydrogenase of rat mammary gland
Biochemical Society transactions, 1975
After the placenta is lost at parturition the concentration of placental lactogen in the blood declines rapidly (Grumbach et al., 1968), whereas that of prolactin shows a compensatory increase. I assume that this switch in lactogenic hormone results in a fall in 'anti-insulin' activity, a situation which would occur if either the serum concentration of prolactin were lower than that of placental lactogen (Hwang et al., 1971) or if prolactin were inherently less like growth hormone (Niall et al., 1971). Hence the restraint on carbohydrate metabolism is removed and milk synthesis proceeds. The idea of negative rather than positive control of the initiation of milk synthesis has previously been considered for progesterone, whose concentration also falls at parturition (Kuhn, 1971). Although progesterone probably regulates the switch from placental to pituitary lactogen, the possibility that it has a direct inhibitory effect on the mammary gland seems less likely. Thus although progesterone does inhibit the induction of alactalbumin in vitro, its effect appears to be specific to this protein, other proteins being unaffected (Turkington &Hill, 1969; Leader &Barry, 1969) In contrast, the hypothesis I propose suggests a way in which a single hormone, placental lactogen, through its separate biochemical effects on carbohydrate metabolism and specific protein synthesis might exert a general restraint on the synthesis ofmilk constituents, while simultaneously promoting growth and differentiation of the milk-producing tissue.
Reproduction, 1986
Administration of progesterone (5 or 10 mg) to pregnant rats increased serum prolactin significantly on the afternoon of Days 4, 6, 7 and 8 of pregnancy, but had no effect on later days. On Day 10 progesterone administration increased serum prolactin only in rats treated with oestrogen the day before. A similar treatment with oestrogen and progesterone was unable to stimulate secretion on the afternoon of Day 13 of pregnancy. In rats from which the corpora lutea had been unilaterally removed and hence endogenous progesterone levels were 50% of the normal values, or in those that carried 4 conceptuses, progesterone treatment after oestradiol priming was partly effective in inducing prolactin release on Day 13. However, in rats ovariectomized, with bilateral excision of the corpora lutea, or with 2 conceptuses left, treatment with ovarian steroids markedly increased serum prolactin values. By Day 13 all the rats from the ovariectomized group or with bilateral excision of the corpora lutea had aborted. On Day 13, therefore, the high serum concentrations of feto-placental factors and of progesterone are responsible for the blockade of the spontaneous and ovarian steroid\x=req-\ induced prolactin release. On the other hand, on Day 16 of pregnancy the decrease of circulating progesterone by excision of the corpora lutea or by ovariectomy followed by oestradiol treatment significantly increased serum prolactin on Day 17. Removal of all the conceptuses did not modify the effects of these treatments.
Glucocorticoids and Progesterone Prevent Apoptosis in the Lactating Rat Mammary Gland
Endocrinology, 2002
Previous studies have shown that apoptosis in the postweaning mammary gland is substantially reduced by treatment with glucocorticoids or progesterone, but whether these steroids exert a similar antiapoptotic effect during normal lactation is not known. Therefore, the present study used an in vivo rat model to assess the effects of progesterone and glucocorticoids on apoptosis in the lactating mammary gland. Rats were untreated, sham operated, ovariectomized (OVX), and/or adrenalectomized (ADX) on d 10 of lactation. Additional groups of OVX/ADX rats were treated with either progesterone or corticosterone. Mammary gland apoptosis was determined 3 d later by 3-end labeling of fragmented DNA and by in situ terminal deoxynucleotidyl transferasemediated deoxyuridine triphosphate biotin nick end label-ing analysis (TUNEL). DNA fragmentation was relatively low in the mammary gland from untreated and sham-operated rats and was unaffected by either ADX or OVX alone. In contrast, DNA fragmentation was markedly elevated in OVX/ADX rats (P < 0.01), but this effect on mammary gland apoptosis was prevented by replacement with either corticosterone or progesterone. Consistent with these data, dying cells identified by TUNEL analysis were readily observed in the alveolar epithelium of mammary tissue from OVX/ADX rats but not in any of the other groups. These data demonstrate that during normal lactation, mammary gland apoptosis is inhibited by endogenous progesterone and glucocorticoids. Importantly, the presence of either steroid alone was sufficient to prevent apoptosis, suggesting that their antiapoptotic effects in the lactating mammary gland may be mediated via similar signaling pathways.
Variations in the cellular proliferation of prolactin cells from late pregnancy to lactation in rats
Annals of Anatomy - Anatomischer Anzeiger, 2003
Lactation is a physiological process associated with hyperactivity of hypophyseal prolactin-producing cells. It is known that the percentage of these cells is increased during lactation, although there are discrepancies in the reports regarding the mechanisms responsible for increasing the number of prolactin cells. In order to analyse whether this increase is a result of previous proliferation, variations in the proliferation rate of prolactin-positive cells were determined from late pregnancy to lactation in adult female rats by means of observation of the immunohistochemical expression of PCNA as a marker of cellular proliferation. During late pregnancy, a very significant increase in the percentage of proliferating prolactin cells was observed in comparison to non-pregnant females in the proestrus phase (p<0.01). Although the percentage of prolactin-positive cells after one week of lactation was