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N. J. KUHN

SUMMARY

Lactogenesis, as indicated by the appearance of mammary lactose, follows ovariectomy and/or hysterectomy and the fall in the concentration of progesterone in the plasma preceding normal parturition in the pregnant rat. It is suppressed by administered progesterone in all cases, and by prolactin after hysterectomy.

The natural lactogenic signal may occur 30 hr. before parturition, due to conversion of progesterone to 20α-hydroxypregn-4-en-3-one in the ovaries. Changes in the concentration of corticosterone, oestrogen and prolactin in the plasma either do not occur or do not constitute a lactogenic signal.

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N. J. KUHN

The hormonal control of lactogenesis has recently been studied by specific chromatographic or enzymic measurements of mammary lactose which have superseded earlier assessments of retained milk or alveolar 'secretory' granules (Chadwick, 1962; Shinde, Ôta & Yokoyama, 1964; Kuhn, 1969). Because lactose is not necessarily representative of other milk solids, protein phosphorus was measured to assess changes in rat mammary casein during lactogenesis.

Wistar-derived rats were used during their first pregnancy or lactation. Mammary tissue was dissected out, pulverized under liquid nitrogen and about 0·8 g was accurately weighed into a round-bottomed glass centrifuge tube. The powder was triturated successively with two 8 ml vols of acetone to remove fat, and with five 8 ml vols of a mixture of chloroform:methanol:conc. HCl (200:100:1, by vol.) to remove phospholipid (Teng, Teng & Allfrey, 1971). After a further extraction with 8 ml acetone the residue was extracted with 8 ml 5% (w/v) trichloroacetic

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N. J. KUHN

The withdrawal of ovarian progesterone either naturally at the end of pregnancy, or after ovariectomy, hysterectomy, or both, leads to a rapid accumulation of lactose in the mammary gland of the rat in late pregnancy (Shinde, Ôta & Yokoyama, 1965; Kuhn, 1969). In each instance administered progesterone prevents this accumulation (Kuhn, 1969; R. P. Deis & A. Alonso, quoted by Deis, 1968). The natural disappearance of progesterone before parturition is paralleled by a marked rise in the concentration of 20α-hydroxypregn-4-en-3-one in the plasma (Fajer & Barraclough, 1967; Hashimoto, Hendricks, Anderson & Melampy, 1968; Wiest, Kidwell & Balogh, 1968; Kuhn, 1969), due to the appearance of 20α-hydroxysteroid dehydrogenase in ovarian corpora lutea (Wiest et al. 1968; N. J. Kuhn & M. S. Briley, to be published). To support the concept of progesterone withdrawal as a physiological trigger for lactogenesis (Kuhn, 1969) it is necessary to show that closely related steroids, especially

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STELLA Y. KYRIAKOU and N. J. KUHN

The transition of the mammary gland from the quiescent state of pregnancy to the secretory state characteristic of lactation requires the presence of several hormones. Thus, when lactogenesis in rats or mice is monitored by increases of mammary lactose or casein, or of biosynthetic enzymes such as lactose synthetase, it shows a minimum requirement for prolactin and corticosteroid. Cultured mammary explants from pregnant mice undergo similar changes when given a minimum hormonal supplement of insulin, prolactin and a corticosteroid (for review see Denamur, 1971). The insulin is required in vitro at high concentrations (about 50 mu./ml) and apparently stimulates a wave of cell division from which the daughter cells undergo 'functional differentiation' in the presence of the other two hormones (for review see Topper, 1968, 1970). Lactogenesis in vivo is accompanied or preceded by active mitosis according to some authors (Jeffers, 1935; Baldwin & Milligan, 1966) but not according to

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A. LORRAINE OWEN and N. J. KUHN

Recent studies have shown that progesterone 'withdrawal' in the pregnant rat, which is essential for normal parturition (Nelson, Pfiffner & Haterius, 1930; Stucki & Forbes, 1960) and for lactogenesis (Kuhn, 1969a), is due to a decrease in the rate of ovarian progesterone secretion (Fajer & Barraclough, 1967; Hashimoto, Hendricks, Anderson & Melampy, 1968). This in turn is largely due to a rapid increase of 20α-hydroxysteroid dehydrogenase activity in the ovary which redirects the metabolism of pregnenolone away from progesterone towards 20α-hydroxypregn-4-en-3-one, which is secreted in its place but which is hormonally inactive (Wiest, 1968; Wiest, Kidwell & Balogh, 1968; Kuhn, 1969b; Kuhn & Briley, 1970). The present communication gives evidence for a similar change in pregnenolone metabolism near parturition in the mouse ovary.

Mice of strain LACA/B/AC (Oxfordshire Laboratory Animal Colonies, Bicester, Oxon.) were mated over a period of 1 or 3 days. Litters were born on day

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DAVID HICKMAN-SMITH and N. J. KUHN

SUMMARY

Luteolysis was induced in rats during late pregnancy by fetoplacental removal, and was monitored by the increased activity of luteal 20α-hydroxysteroid dehydrogenase (20α-OHSDH). The extent of enzyme induction over a given length of time varied according to the time of day at which the fetuses and placentae were removed, 11.00 and 21.00 h appearing to give optimal and minimal enzyme activities respectively. The 20α-OHSDH was more readily induced on day 19 than on day 18.

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R. Peeters, N. Buys, D. Vanmontfort, J. Van Isterdael, E. Decuypere and E. R. Kühn

ABSTRACT

The influence of TRH and TSH injections on plasma concentrations of tri-iodothyronine (T3) and thyroxine (T4) was investigated in neonatal (injection within 0·5 h after delivery) and growing lambs and in normal, pregnant and lactating adult ewes (all 2 years old and originating from Suffolk, Milksheep and Texal cross-breeds). Neonatal lambs had higher levels of T3, T4 and GH compared with all other groups, whereas prolactin and TSH were higher in lactating ewes. In all animals, injections of TRH increased plasma concentrations of prolactin and TSH after 15 min but not of GH at any time. Small increases in T3 and T4 were observed in neonatal lambs, without any effect on the T3 and T4 ratio, after prolactin administration, whereas prolactin did not influence plasma concentrations of T3 or T4 in all other experimental groups. Similar results for thyroid hormones were obtained after TRH or TSH injections. It was therefore concluded that the effects observed after TRH challenge were mediated by the release of TSH. With the possible exception of neonatal lambs, plasma concentrations of T3 after administration of TRH or TSH were always increased before those of T4; the increase in T3 occurred within 0·5–1 h compared with 2–4 h for T4 in all experimental groups. This resulted in an increased ratio of plasma T3 to T4 up to 4 h after injection. It is concluded that, in sheep, TRH and TSH preferentially release T3 from the thyroid gland probably by a stimulatory effect of TSH on the intrathyroidal conversion of T3 to T4.

Journal of Endocrinology (1992) 132, 93–100