bluuebunny/crossref_metadata_2025_split huggingface dataset:
Specific binding sites for progesterone in subcellular fractions of the porcine corpus luteum
Authors: Menzies G S , Bramley T A 
Published: December 2008

Abstract
Subcellular fractionation of porcine corpus luteum (CL) homogenates on continuous sucrose gradients has previously demonstrated that most of the endogenous progesterone of the CL was associated with a unique particulate fraction. Exogenous radiolabelled steroids were also sequestered with some specificity by this fraction. We now report that this particulate fraction is capable of binding high levels of exogenous 3H-labelled progesterone (and pregnenolone) in vitro, but only in the presence of the saponin, digitonin. Binding was dependent on the pH, temperature and duration of incubation, and showed specificity and high affinity for progesterone (Kd, 79 nm). Androgens, oestrogens and pregnenolone competed for porcine luteal [3H] progesterone binding sites, but only at much higher concentrations, whereas cholesterol, a number of progesterone receptor agonist and antagonist analogues and inhibitors of 3β-hydroxysteroid dehydrogenase and C17-hydroxylase/C17,20-lyase did not compete.
Analysis of profiles for a number of luteal cell-surface membrane and intracellular organelle markers confirmed previous studies showing the association of an NADH-cytochrome C reductase with this fraction. Moreover, the content of endogenous progesterone associated with particulate subcellular fractions isolated from porcine granulosa cell (GC) and CL homogenates at different stages of the luteal phase and early pregnancy waxed and waned with the stage of the luteal phase (and the secretory activity of the CL). Binding of [3H]progesterone in vitro equilibrated at the same buoyant density as endogenous progesterone: levels of both were highest during the mid-luteal phase and during early pregnancy, lower in early and late luteal CL, and undetectable in corpora albicantia. In contrast, relaxin secretory granules were readily resolved from progesterone binding sites. We propose that these particulate progesterone binding sites may be involved in the sequestration and/or packaging of newly-synthesized steroid for secretion by the luteal cell, or may mediate actions of progesterone within the luteal cell.
Journal of Endocrinology (1994) 142, 101–110
The influence of thyroid hormones on the growth of the atria and ventricles of the heart in immature rats
Authors: Canavan J P , Holt J , Goldspink D F 
Published: December 2008

Abstract
The normal plasma concentrations of tri-iodothyronine (T3) and thyroxine (T4) increase approximately six- and fourfold respectively between the end of gestation and weaning in the rat. This early postnatal surge of thyroid hormones was experimentally modified to produce either a state of hypo- or hyperthyroidism. The growth and rates of protein turnover in the atria and ventricles of the heart were studied, 12 and 20 days postpartum, both as a function of age and of changing thyroid status.
Neonatal hypothyroidism was induced by adding propylthiouracil to the mothers' drinking water late in gestation and throughout lactation. Hyperthyroidism was achieved by giving the suckling pups daily injections of T4 from day 3 postpartum onwards.
Between 12 and 20 days the weight and protein mass of the combined ventricles of the euthyroid animals approximately doubled, along with substantial increases (50%) in the RNA and DNA contents. Over this same 8 days, growth in the combined atria was much slower. During the same period, hypothyroidism significantly retarded the growth of these immature rats and their atria and ventricles. Both the rates of protein synthesis and protein degradation were decreased in the atria and ventricles. In contrast, hyperthyroidism significantly increased growth in both types of cardiac tissue, this being more pronounced in the atria than in the ventricles between 12 and 20 days. The rates of protein synthesis were increased accordingly, principally by increases in the ribosomal activities.
In conclusion, thyroid hormones clearly influence the early postnatal growth of the atria and ventricles of the heart in the rat.
Journal of Endocrinology (1994) 142, 171–179
The effects of ovarian transplantation on bone loss in ovariectomized rats
Authors: Tobias J H , Chambers T J , Gallagher A 
Published: December 2008

Abstract
Although hormone replacement therapy can prevent postmenopausal bone loss, it does not restore bone mass to normal in patients with established osteoporosis. This might reflect a failure to reproduce certain aspects of gonadal function. One method of investigating this possibility would be to examine the effect of ovarian transplantation on the skeleton of osteopaenic ovariectomized rats. However, ovarian transplantation may not fully restore ovarian function to normal, and it is not known whether transplanted ovaries reproduce the action of native ovaries on the skeleton. Therefore, we investigated whether renal capsular or subcutaneous ovarian transplants prevent the effects of ovariectomy on histomorphometric indices of rat tibiae over 44 days. Daily vaginal smears showed that oestrous cycles returned in all but two of 25 animals receiving ovarian transplants. We found that ovarian transplantation prevented the reduction in cancellous bone volume following ovariectomy. While trabecular number was reduced in ovariectomized animals receiving renal capsular ovarian transplants compared to intact animals, trabecular thickness was increased in both transplant groups. Ovarian transplantation also prevented the increase in cancellous and cortical bone formation, cancellous bone resorption and longitudinal growth rate caused by ovariectomy. We conclude that restoration of ovarian function by ovarian transplantation largely prevents the effects of ovariectomy on histomorphometric indices of rat tibiae, suggesting that transplanted ovaries can substitute for the action of native ovaries on the skeleton.
Journal of Endocrinology (1994) 142, 187–192
Effects of ovariectomy and oestradiol replacement on hypothalamic serotonergic and monoamine oxidase activity in the catfish, Heteropneustes fossilis: a study correlating plasma oestradiol and gonadotrophin levels
Authors: Senthilkumaran B , Joy K P 
Published: December 2008

Abstract
Hypothalamic serotonin (5-HT; content and turnover) and monoamine oxidase (MAO) activity were measured in female catfish, Heteropneustes fossilis, after ovariectomy and supplementation with oestradiol-17β (OE2) in the recrudescent and quiescent phases. These factors were correlated with changes in plasma levels of OE2 and gonadotrophin. In the quiescent phase (December), neither ovariectomy nor OE2 supplementation had any significant effect on 5-HT content and MAO activity. Plasma levels of OE2 and gonadotrophin were undetectable in both control and treated fish, indicating that there was no feedback effect. In the recrudescent phase (prespawning, May), ovariectomy caused biphasic responses of MAO activity and 5-HT content. The enzyme activity decreased significantly after 2, 3, 4 and 5 weeks but increased significantly 6 weeks after ovariectomy. The 5-HT content varied in a biphasic manner with a significant increase at 2, 3 or 4 weeks and a significant decrease in week 6; there being no effect in week 5. 5-HT turnover was inhibited significantly only in week 4 after ovariectomy and did not show a biphasic pattern. In the ovariectomized groups, the OE2 level decreased significantly in a progressive manner with a maximum reduction in week 6. The plasma level of gonadotrophin showed a significant bimodal pattern of increase with the peak in week 4 after ovariectomy, indicating a strong negative feedback effect of OE2. The bimodal pattern of pituitary gonadotrophin release could be correlated with a similar pattern of increase in 5-HT content. OE2 treatment of fish which had been ovariectomized 3 weeks previously had dose-dependent effects on the enzyme; the low dose (0·1 μg/g body weight) was stimulatory and the higher doses (0·5, 1·0 and 5·0 μg/g body weight) were inhibitory. The reverse was true for 5-HT content. Serotonergic turnover increased significantly only in the groups given high doses (1·0 and 5·0 μg/g body weight). The low dose of OE2 (0·1 μg/g body weight) restored the gonadotrophin and OE2 levels to those of the sham-ovariectomized vehicle-treated control group, whereas the high doses (0·5, 1·0 and 5·0 μg/g body weight) decreased the release of gonadotrophin in a dose-dependent manner. Our results suggest that OE2 modulates MAO activity to alter hypothalamic 5-HT in a seasonally dependent manner. The ovariectomy-induced changes in plasma levels of gonadotrophin appear to be mediated, at least partly, by the feedback action of OE2 on 5-HT metabolism.
Journal of Endocrinology (1994) 142, 193–203
Tissue distribution and regulation of 5′-deiodinase processes in lactating rats
Authors: Jack L J W , Kahl S , Germain D L St , Capuco A V 
Published: December 2008

Abstract
Thyroxine 5′-deiodinase (5′D) catalyses deiodination of the prohormone thyroxine (T4) to the metabolically active hormone 3,5,3′-tri-iodothyronine (T3). Previously, it has been demonstrated that rat mammary gland expresses a 5′D with enzymatic properties equivalent to those of the type I enzyme (5′D-I) found in rat liver and kidney. Using complementary DNA (cDNA) for rat hepatic 5′D-I, we have examined expression of 5′D-I messenger RNA (mRNA) in liver, and mammary gland from virgin and lactating rats, and in seven other tissues from virgin rats. 5′D-I mRNA could not be detected in mammary gland either by Northern blotting or by the more sensitive technique of reverse transcribing mRNA and then amplifying the cDNA by polymerase chain reaction (RTPCR). Analysis of the seven tissues from virgin rats by RT-PCR showed 5′D-I amplicons in liver, kidney and thyroid. No amplicons were detected in adrenal gland, cardiac muscle, skeletal muscle or spleen. In addition, the effect of lactation intensity on circulating thyroid hormones, hepatic and mammary gland 5′D activity, and hepatic 5′D-I mRNA levels was examined. A strong inverse relationship was noted between increased lactation intensity (suckling burden) and circulating T4 and T3, hepatic 5′D-I activity and hepatic 5′D-I mRNA levels. Mammary gland 5′D activity was positively correlated to lactation intensity. The data presented strongly suggest that the 5′D activity expressed in lactating mammary gland is encoded by a mRNA different from the 5′D-I message found in rat liver, kidney and thyroid gland, and may help explain the differential regulation of 5′D-I activity in these organs during lactation. In addition, hepatic 5′D-I activity was found to be correlated with the concentration of 5′D-I mRNA, suggesting that regulation is pretranslational. Results are consistent with a previously suggested involvement of 5′D in establishing metabolic adaptations to support lactation.
Journal of Endocrinology (1994) 142, 205–215
Parathyroid hormone-related protein in human term placenta and membranes
Authors: Bowden S J , Emly J F , Hughes S V , Powell G , Ahmed A , Whittle M J , Ratcliffe J G , Ratcliffe W A 
Published: December 2008

Abstract
Parathyroid hormone-related protein (PTHrP), the hypercalcaemia of malignacy factor, is expressed in the tissues of the human uteroplacental unit, including the placenta, amnion and chorion. We have used three region-specific immunoassays to quantitate and compare the distribution of PTHrP in tissues obtained at term following spontaneous labour and vaginal delivery or elective Caesarean section. In non-labouring women highest PTHrP(1–86) and (37–67) immunoreactivity was found in amnion covering the placenta, rather than the decidua parietalis of the uterus (reflected amnion) (median 1020 vs 451 fmol/g; 2181 vs 1444 fmol/g respectively). In labouring women, the PTHrP(1–86) concentration in reflected amnion was inversely correlated with the interval between rupture of the membranes and delivery. Tissue PTHrP(1–86) concentrations were lower in placenta than in chorion and amnion (medians 12, 109 and 664 fmol/g respectively) and, in all tissues, PTHrP(1–34) and (37–67) concentrations were significantly higher than that of PTHrP(1–86). Bioactive PTHrP(1–34) was detected in placenta, chorion and amnion using the ROS cell bioassay. The PTHrP(1–86) concentration (mean ± s.e.m.=41·4 ± 4·5 pmol/l) was high in amniotic fluid at term, although in maternal and cord plasma levels were only modestly increased. The molecular forms of PTHrP present in tissues and amniotic fluid were investigated by column chromatography which confirmed its molecular heterogeneity and suggested that processing is tissue-specific and occurs at both amino- and carboxy-terminals of the peptide.
Journal of Endocrinology (1994) 142, 217–224
Internalization of metformin is necessary for its action on potentiating the insulin-induced Xenopus laevis oocyte maturation
Authors: Khan N A , Wiernsperger N , Quemener V , Moulinoux J-P H 
Published: December 2008

Abstract
In this study, metformin (N, N1 dimethylbiguanide) was found to potentiate insulin-induced Xenopus laevis oocyte maturation, a phenomenon of transition from late G2 to M phase of the cell cycle. These cells also accumulated exogenous metformin (130 ± 6·5 nmol/oocyte). Metformin covalently-coupled to Sepharose 4B beads failed to potentiate the insulin-induced oocyte maturation which suggests that these cells did not take up metformin from the extracellular medium. Addition of metformin alone to Xenopus laevis oocytes did not induce the maturation process, though these cells took up exogenous metformin. Micro-injection of metformin (120 nmol/oocyte) to oocytes accelerated the insulin-induced maturation, but it was lower than in cells which were incubated with free metformin together with insulin. Interestingly, insulin had no effect on metformin uptake by the oocytes. Methylglyoxal-bis(guanylhydrazone), MGBG, an apparent analogue of metformin, induced oocyte maturation. Addition of metformin, either free or Sepharose-bound, did not influence the MGBG-induced 60% maturation of Xenopus laevis oocytes. These results suggest that the internalization of metformin is necessary for its action and its effects are specific on insulin activity.
Journal of Endocrinology (1994) 142, 245–250
Levels of insulin-like growth factor-binding protein-2 and insulin-like growth factor-II in maternal serum, amniotic fluid and extraembryonic coelomic fluid at 9–20 weeks of pregnancy
Authors: Chard T , Blum W F , Brunjes J , Campbell D J , Wathen N C 
Published: December 2008

Abstract
Insulin-like growth factor-II (IGF-II) and IGF-binding protein-2 (IGFBP-2) were measured in amniotic fluid, extraembryonic fluid and maternal serum from 20 women with apparently normal first trimester pregnancies prior to termination. A further 111 specimens of amniotic fluid were collected from women at 10–20 weeks of pregnancy. Levels of IGFBP-2 were similar in coelomic fluid and maternal serum. Levels in amniotic fluid were lower than those in serum and coelomic fluid (Mann–Whitney test; P=0·0002 and P<0·0001 respectively). The levels of IGF-II were much higher in maternal serum than in coelomic fluid, and higher in the latter than in amniotic fluid (Mann–Whitney test; P<0·0001 for both situations). The levels of IGFBP-2 were relatively low at 10–11 weeks (medians 19·8 and 61·1 μg/l) but thereafter increased to 20 weeks (median 1400 μg/l). The levels of IGF-II showed a similar pattern. The findings suggest that the role of IGF-II and IGFBP-2 in the regulation of growth or differentiation of the fetus or of its surrounding membranes may change with advancing pregnancy.
Journal of Endocrinology (1994) 142, 379–383
Endothelin in the human uterus during pregnancy
Authors: Maggi M , Vannelli G B , Fantoni G , Baldi E , Magini A , Peri A , Giannini S , Gloria L , Del Carlo P , Casparis D , Tomei T , Serio M 
Published: December 2008

Abstract
In this study we report the immunolocalization, binding and biological activity of endothelins in the human uterus. Since, in previous studies in the rabbit, sex steroids greatly affected uterine endothelin-1 (ET-1) immunolocalization and binding, we sought to compare results obtained in a relatively steroid-deprived uterus (postmenopausal women) with those obtained in late pregnancy. Two classes of ET receptors were identified in human pregnant and non-pregnant myometrium. One site (ETB) was a low capacity site (0·3 pm/mg protein) that bound with high affinity (0·1 nm), yet no selectivity, ET-1, ET-2, ET-3, sarafotoxin (SRTX) and vasoactive intestinal contractor (VIC). The second site (ETA) was six fold more concentrated than the former (1·9 pm/mg protein) and was relatively selective for ET-1, ET-2 and VIC but showed lower affinity for ET-3 and SRTX. Studies with human myometrial cells indicated that the ETA receptor mediates an increase in intracellular calcium, while the physiological function of the ETB receptor is still unclear. Homologous competition curves for ET-1 were used in order to study the ET receptor density (ETA+ETB) in individual myometrial samples. We found that the concentration of ET receptors did not change during different stages of labour or in postmenopausal women. We identified cells with intense positivity for ET-1 in human decidua. Similar cells were also present in pregnant myometrium, intimately associated with smooth muscle cells. Conversely, no staining for ET-1 was observed in non-pregnant myometrium. A paracrine role for ET-1 in the human uterus is suggested.
Journal of Endocrinology (1994) 142, 385–396
Transport stress delays the oestradiol-induced LH surge by a non-opioidergic mechanism in the early postpartum ewe
Authors: Smart D , Forhead A J , Smith R F , Dobson H 
Published: December 2008

Abstract
The present study was designed to investigate whether transport, a mild environmental stressor, could affect the oestradiol-induced LH surge in postpartum ewes and, if so, the mechanism involved. Welsh Mountain ewes, with lambs removed at parturition (day 0) and hand-milked 12 and 48 h later, were given 50 μg oestradiol benzoate intramuscularly at various times postpartum. Blood samples were taken via an indwelling jugular venous catheter every 2 h from 8 to 24 h after oestradiol injection. All results are given as means ± s.d. On day 1 oestradiol was unable to induce an LH surge in any ewe. Transport (10–14 h after oestradiol) delayed the onset of the oestradiol-induced LH surge on day 14 (17·5 ±1·7 vs 14·4±2·0 h, n=5 each; P<0·05), but not on day 28 (14·9 ±2·0 vs 14·0 ±2·4 h, n=5 out of 7). Transport had no effect on the amplitude of the surge on either day. Naloxone treatment (1 mg/kg per 2 h) was unable to prevent the delay caused by transport (18·0±1·1 vs 17·5 ± 1·7 h, n=8 each), and did not affect the amplitude of the surge (28·4±5·3 vs 28·1 ±2·3 ng/ml, n=8 each). The duration of the LH surges were not assessed. On day 7, transport from 16 to 20 h after oestradiol delayed the LH surge (22·8 ±2·0 vs 18·0 ± 2·8 h, n=8 each; P<0·05) and reduced the surge amplitude (19·7 ±1·7 vs 22·8 ±2·8 ng/ml; P<0·05), whilst transport from 10 to 14 h did not. Transport (16 to 20 h) had no effect on surge duration (6·25 ±0·7 vs 6·75 ± 1·0 h). In conclusion, transport inhibited the oestradiol-induced LH release in the early postpartum ewe by a non-opioidergic mechanism, but only if the stressor occurred within 2–3 h of the expected onset of the surge.
Journal of Endocrinology (1994) 142, 447–451
Tissue-specific regulation of the growth hormone receptor gene in streptozocin-induced diabetes in the rat
Authors: Menon R K , Stephan D A , Rao R H , Shen-Orr Z , Downs L S , Roberts C T , LeRoith D , Sperling M A 
Published: December 2008

Abstract
Abnormalities of GH secretion and clearance are well-documented in poorly controlled insulin-dependent diabetes mellitus (IDDM), but the contribution of the receptor (GHR) and the GH-binding protein (GHBP) to these abnormalities has not been defined. We studied the expression of the GHR/GHBP gene in the livers, hearts and kidneys in streptozocin-induced diabetes (STZ-D) in the rat. GHR and GHBP mRNA levels were measured by Northern blot and ribonuclease protection assays. Whereas levels of GHR and GHBP mRNA were significantly decreased in liver and heart of STZ-D rats when compared with the control group (P<0·01), GHR mRNA was significantly increased in the kidneys of STZ-D rats (P=0·03). Six days of insulin treatment did not significantly alter the levels of GHR/GHBP mRNA in the liver or heart of STZ-D rats, but significantly decreased GHBP mRNA (P=0·04) in the kidney. Circulating IGF-I was reduced, as was IGF-I mRNA in the liver and heart of STZ-D rats; only circulating IGF-I was restored by insulin treatment. Neither STZ-D nor insulin treatment affected IGF-I or IGF-I receptor mRNA concentrations in the kidney. We conclude that (1) STZ-D modulates the expression of the GHR/GHBP gene and (2) that these changes in GHR/GHBP mRNA concentrations are tissue-specific; STZ-D decreases GHR/GHBP mRNA in liver and heart tissue but increases GHR mRNA concentrations in the kidney. Our results indicate a role for decreased numbers of hepatic GHRs in the pathogenesis of resistance to GH's actions in terms of IGF-I generation and promotion of linear growth in IDDM. We postulate that increased GHR expression in the kidney may be involved in the renal complications of IDDM.
Journal of Endocrinology (1994) 142, 453–462
PITUITARY ADENYLATE CYCLASE-ACTIVATING PEPTIDE-38 (PACAP)-38 IS RELEASED INTO HYPOPHYSIAL PORTAL BLOOD IN THE NORMAL MALE AND FEMALE RAT
Authors: Dow R C , Bennie J , Fink G 
Published: December 2008

ABSTRACT
Pituitary adenylate cyclase activating polypeptide (PACAP) was first isolated from ovine hypothalamus as two molecular forms, the basic 38 residue amidated peptide PACAP-38 and the N-terminal 27 amino acid sequence PACAP-27. A dense plexus of PACAP immunoreactive fibres is present in the internal and external layers of the median eminence and in other parts of the hypothalamus with PACAP cell bodies in the paraventricular and supraoptic nuclei. The present study shows, for the first time, that, as assessed by radioimmunoassay of extracted plasma, the amount of PACAP-38 in hypophysial portal is significantly greater than in peripheral blood, and that as assessed by reversed phase high performance liquid chromatography, PACAP 1-38 is the major form in portal blood. This evidence is crucial for the fact that PACAP-38 may be a hypothalamic-pituitary regulatory factor.