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, Rechler & Clemmons 1998 , Bunn & Fowlkes 2003 ). One of these proteases was identified as pregnancy-associated plasma protein-A (PAPP-A) ( Lawrence et al. 1999 ). PAPP-A has been shown to cleave inhibitory IGFBP-4 and consequently increase the IGF
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SUMMARY
Lipids in the uterine endometrium of mice during early pregnancy were investigated by histochemical techniques. Three groups of animals were studied: (1) on days 1–8 inclusive of the first pregnancy, (2) on days 1–9 after mating at the post-partum oestrus and suckling seven or eight young from their first pregnancy, (3) on days 1–6 after delivery of the first litter but with no access to males. Day 1 was that on which a seminal plug appeared in the vagina or (group 3) after birth of a litter during the previous night. In post-partum mice, only the areas between the former implantation sites were studied.
Epithelial lipids are sparse during the first 24 h. On day 2 and early day 3 in nulliparous mice, and for a longer period in post-partum mice, the presence of lipid in epithelium and stroma seems mainly a degenerative phenomenon associated with cell breakdown and consequent tissue disruption. During late day 3 and on day 4 the increase in lipid droplets giving staining reactions characteristic for triglycerides may represent the storage in this form of fatty acids no longer needed for phospholipid synthesis or as energy sources, once the intense mitotic proliferation of these cells dies down. Triglycerides also predominated in the necks of the glands, but in the deeper parts, the sparse droplets often gave staining reactions for acidic lipids. In differentiating decidual cells during day 5 and early day 6 in nulliparous mice, histochemical reactions suggest that fatty acids accumulate. Some of these are probably utilized in synthesis of the increasing amounts of phospholipids which were particularly prominent later on day 6 and during day 7, while others appeared to be temporarily stored during that period as triglycerides. The phased deposition and removal of triglyceride proceeds centrifugally through the decidua and is slightly in advance of glycogen deposition and removal in the same cells; its time-course correlated well with that which other workers have described from chemical assay. Histochemical tests appeared to reveal activity of a lipase-esterase (fatty acid ester hydrolase) which strengthened and spread through the decidua in parallel with the disappearance of lipid droplets. In lactating mice, as long as the blastocysts remained in diapause, epithelial lipid resembled that on day 4; in the stromal cells, lipid droplets were plentiful in areas close to the former placental sites but were few or absent elsewhere. Once the delayed implantation had started no abnormalities were detected. Alterations in lipids are discussed in the context of the known changes in the levels of ovarian hormones. Lipids within uterine macrophages are also discussed.
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We have recently demonstrated the existence of a neuromodulatory regulation of prolactin secretion by the opioid system showing a paradoxical opioid-induced prolactin suppression at the end of pregnancy. The aim of this study was to determine a possible interaction between the opioid system and ovarian hormones on the release of prolactin during pregnancy. Serum prolactin levels measured at 1800 h were significantly higher on days 3 and 6 of pregnancy when compared with the other days of gestation. These increases in serum prolactin were reduced significantly by naloxone (2 mg/kg) administered at 1730 h and by RU-486 (10 mg/kg) administered at 0800 h. The response induced by RU-486 was potentiated by naloxone only on day 3. On days 7, 13 and 16, prolactin secretion was not modified by RU-486 and/or naloxone treatment. In RU-486 pretreated rats, naloxone administration increased serum prolactin levels only on day 16 of pregnancy. Interestingly, progesterone treatment (0.5 mg/rat) on days 13, 14 and 15 of pregnancy prevented the high increase in serum prolactin induced by RU-486 and naloxone on day 16 of pregnancy. The progressive increase and decrease of serum progesterone concentration during pregnancy was not modified by naloxone treatment. The participation of oestrogen in the regulation of prolactin secretion by the opioid system on days 3, 16 and 19 was examined by treating these groups of rats with oestradiol benzoate or tamoxifen citrate. Oestradiol (2 micrograms/rat) significantly increased serum prolactin levels on day 3 and naloxone administration did not modify this increase. No effect was observed after oestradiol (5 micrograms/rat) and naloxone treatment on days 16 and 19 of pregnancy. Oral administration of tamoxifen (500 micrograms/kg) the previous day did not modify the serum prolactin concentration measured at 1800 h in oil-treated rats on days 3, 16 and 19 of pregnancy. The antioestrogen completely abolished the naloxone-induced prolactin secretion on day 16 in rats pretreated with RU-486 but no effect was observed on day 19. When tamoxifen was administered on days 14 and 15 of pregnancy, the high serum prolactin levels on day 19 induced by treatment with RU-486 and naloxone were significantly reduced. In conclusion, these results provide an important new insight into the existence of a dual neuromodulatory regulation of prolactin secretion by the opioid system during pregnancy. After a stimulatory action during the first days, there is a change to an inhibitory control at the end of pregnancy, starting around day 16. Moreover, the activation of the inhibitory modulation of the opioid system on prolactin secretion on days 16 and 19 of pregnancy seems to be mediated by changes in the oestrogen and progesterone action.
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Abstract
Anti-progesterone treatment using specific anti-progesterone antibodies or a progesterone receptor (PR) antagonist during first pregnancy impairs postpartum maternal behaviour in mice. This effect is demonstrable only if the treatment is given during pregnancy but not immediately after parturition. The purpose of the present studies was to investigate if maternal behaviour is also impaired by anti-progesterone treatment in subsequent pregnancies.
Studies with a monoclonal antibody to progesterone (DB3; 4·5 nmol/mouse) showed that injection of females on day 17 of second pregnancy did not cause maternal rejection but the latency of pup retrieval was prolonged especially during the first 3 days of lactation. This phenomenon was not observed in animals that had previous experience of full length lactation. Experiments were carried out with mifepristone (RU486; 10 μg/mouse) injected at day 17 of first, second or third pregnancies. Pup rejection (22·5% vs 12·3%) and prolongation of the retrieval latency (62·3 ± 13·3 vs 19·7 ± 6·5 s; P<0·02) were observed following the first pregnancy. No abnormal behavioural effects were found in mothers treated in second or third pregnancy who had prior full length lactation experience. Control females subjected to only one pup retrieval test after first delivery rejected their pups if treated in their second pregnancy (27.3% vs 4·4%; P<0·001) and displayed a marginal prolongation of the retrieval latency period (20·9 ± 7·0 vs 7·4 ± 2·6 s). Anti-progesterone treatment had no negative influence when administered during third pregnancy.
To determine whether treatment with RU486 (50 μg/mouse, day 17) during first pregnancy has any residual effects, maternal response was monitored after completion of second pregnancy where no treatment was given. Females who exhibited both maternal rejection and prolonged retrieval latency following first pregnancy did not demonstrate any carryover effects during second lactation, indicating that there is no long-term consequence of RU486 treatment. These results suggest that: (i) anti-progesterone treatment of pregnant mice prevents maternal recognition and disrupts postpartum behaviour in females who had no, or very limited, nursing experience; (ii) there is a progesterone-dependent imprinting mechanism during the first pregnancy that is disrupted by anti-progesterone antibody or PR antagonist; and (iii) this imprinting mechanism and first lactation are important components of the consolidation of neural pathways that are associated with the establishment of normal maternal behaviour.
Journal of Endocrinology (1995) 147, 331–337
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criteria of the Australasian Diabetes in Pregnancy Society by either a fasting venous plasma glucose level of ≥5.5 mmol/l glucose, and/or ≥8.0 mmol/l glucose 2 h after a 75 g oral glucose load. Approval for this study was obtained from the Mercy Hospital
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Mammogenesis in primiparous hypophysectomized goats has been assessed between days 60 and 120 of gestation and compared with that found in untreated goats and goats treated with 5 mg bromocriptine/day. There were fivefold increases in the weight of lobulo-alveolar tissue in the hypophysectomized and bromocriptine-treated goats and a tenfold increase in the untreated goats. Histological examination of the mammary glands at 120 days showed normal structure, and determinations of lactose, lactose synthetase, cytosol enzymes, protein, DNA and RNA indicated qualitatively normal initiation of milk synthetic capabilities in both the hypophysectomized and bromocriptine-treated goats. Bromocriptine treatment lowered the plasma concentration of placental lactogen as well as that of prolactin.
The results indicate that placental lactogen has important mammogenic effects during pregnancy.
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Diamond, Rust & Westphal (1969) originally showed that pregnant guinea-pig plasma binds progesterone about 100 times more firmly than cortisol. Work along this line yielded a competitive protein-binding method for the assay of progesterone in plasma during pregnancy.
Plasma was obtained from pregnant Casia guinea-pigs in the latter part of gesta-tion. [1-2-3H]Progesterone (6 ng, 33 Ci/mmol) in ethanol was evaporated to dryness and dissolved in 30 ml 0·04 m-phosphate buffer, pH 7·4. Fifteen microlitres guineapig plasma were added and mixed gently for 1 h at room temperature. To 100 μl plasma, 200 μl methanol were added and the mixture kept at − 20 °C for 10 min. After centrifugation an appropriate volume of the supernatant was transferred to a small glass test tube and evaporated to dryness. Benzene (100 μl) and heptafluorobutyric anhydride (3 μl) were added to the residue and the sample was kept at 62 °C for 30
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Since the pioneer work of Venning & Browne [1937] on pregnanediol excretion a number of attempts have been made to use the estimation of pregnanediol in the urine as a pregnancy test. The earlier workers followed Venning & Browne's method and isolated the glycuronidate from 24 hr. urine specimens [Hain & Robertson, 1939; Wilson & Randall, 1939; Buxton, 1940; Cope, 1940]. These workers reported favourably on the possibilities of the test but the method was laborious and time-consuming; it has also been criticized on purely chemical grounds by Marrian & Gough [1946].
The later method of Astwood & Jones [1941], in which free pregnanediol is isolated after hydrolysis of the urine, presents great technical advantages and was further modified by Talbot, Berman, McLachlan & Wolfe [1941]. This has been called the 'Astwood-Talbot' method by Sommerville, Gough & Marrian [1948] who have just published a further modification of it. Using a
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Circulating growth hormone (GH) concentrations increase in pregnancy and administration of GH during early-mid pregnancy increases fetal growth in well-fed pigs. To determine whether increased maternal GH could promote fetal growth when feed availability is restricted, fifteen cross-bred primiparous sows (gilts) were fed at approximately 30% of ad libitum intake, from mating onwards and were injected daily i.m. with recombinant porcine GH (pGH) at doses of 0, 13.4+/-0.3 and 25.6+/-0.5 microg/kg live weight from day 25 to day 51 of pregnancy (term approximately 115 days). Treatment with pGH increased maternal backfat loss between day 25 and day 51 of pregnancy, and increased maternal plasma IGF-I concentrations measured at day 51 of pregnancy. Fetal body weight, length and skull width at day 51 of pregnancy were increased by maternal treatment with pGH. Fetal plasma glucose concentrations were increased and maternal/fetal plasma glucose concentration gradients were decreased by maternal pGH treatment at 13.4, but not 25.6 microg/kg.day. Fetal plasma concentrations of urea were decreased by both levels of pGH treatment. Overall, fetal weight was negatively correlated with fetal plasma concentrations of urea, positively correlated with maternal plasma alpha-amino nitrogen concentrations and unrelated to glucose concentrations in either maternal or fetal plasma. This suggests that the availability of amino acids, not glucose, limits fetal growth in the first half of pregnancy in underfed gilts, and that maternal GH treatment may improve amino acid delivery to the fetus.
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Pregnancy and progesterone treatment of ovariectomized rats decrease glucose metabolism through the pentose-phosphate pathway in isolated female rat adipocytes. As demonstrated in previous studies, progesterone directly decreases [1-14C]glucose oxidation through the pentose-phosphate pathway and lipogenesis from [6-14C]glucose; the present study therefore compared glucose-induced lipid synthesis during pregnancy (10, 16 and 20 days of pregnancy) with the effect of progesterone treatment (5 mg/rat per day for 14 days) to shed more light on the role of this steroid in glucose metabolism during pregnancy. The inhibition of [6-14C]glucose incorporation into triacylglycerols in the progesterone-treated rats was comparable to that which occurs during late (20 days) and mid-pregnancy (16 days) but not during early pregnancy (10 days). The inhibition of fatty acid synthesis was more important as pregnancy advanced and was different from the decrease in fatty acid synthesis induced by progesterone treatment. The sensitivity to insulin was comparable in virgin, ovariectomized and progesterone-treated ovariectomized rats but not in pregnant rats. This implies that progesterone and insulin affect glucose-induced lipid synthesis by distinct processes and that the impaired glucose metabolism is characterized by a reduction in basal glucose utilization rather than by an impaired insulin response.
