bluuebunny/crossref_metadata_2025_split huggingface dataset:
Kidney insulin-like growth factor-I mRNA levels are increased in postpubertal diabetic rats
Authors: Bach L. A. , Stevenson J. L. , Allen T. J. , Jerums G. , Herington A. C. 
Published: December 2008

ABSTRACT
Diabetes-associated renal enlargement is more marked in postpubertal than prepubertal rats, and in the postpubertal rat, is associated with increased kidney insulin-like growth factor-I (IGF-I) levels for the first 2 days. In order to determine whether local IGF-I production is the cause of this increase in tissue levels, IGF-I mRNA levels were determined in pre- and postpubertal Sprague–Dawley rats made diabetic with streptozotocin (STZ) and in control rats. RNA was extracted from kidneys and livers of rats at 0 h, 6 h, 12 h and days 1, 2, 3 and 7 after STZ injection. After Northern blotting and hybridization with an oligonucleotide probe complementary to an E domain of the IGF-I cDNA, four distinct bands (7·4, 4·8, 1·8 and 1·0 kb) were found. Densitometric analyses of the most prominent bands (7·4 and 1·0 kb), after normalization for 18S ribosomal RNA content, revealed a 50–100% increase in the kidneys of postpubertal diabetic rats compared with postpubertal controls 12 h after STZ injection (P < 0·05, diabetes vs control). Between days 2 and 7, kidney IGF-I mRNA levels in postpubertal diabetic rats fell to approximately 50% of control levels (P < 0·05, diabetes vs control). In contrast, kidney IGF-I mRNA levels in the prepubertal diabetic rats remained unchanged over the 7 days. Liver IGF-I mRNA levels did not rise during the first 24 h and fell to approximately 60% of control levels by day 7 in both pre- and postpubertal diabetic rats (P < 0·05, diabetes vs control). Increased local IGF-I production may underlie the initiation of renal enlargement associated with diabetes mellitus.
Journal of Endocrinology (1991) 129, 5–10
Effect of thyroid hormone on the pre- and post-natal development of the rat testis
Authors: Francavilla S. , Cordeschi G. , Properzi G. , Di Cicco L. , Jannini E. A. , Palmero S. , Fugassa E. , Loras B. , D'Armiento M. 
Published: December 2008

ABSTRACT
The relationship between thyroid function and testicular development in the rat was investigated. Hypothyroidism was induced during fetal or postnatal life by adding methimazole (MMI) to the drinking water of pregnant or lactating mothers. A group of newborn rats was treated with MMI and i.p. injections of l-tri-iodothyronine (l-T3). Hypothyroidism was shown by the reduced serum levels of total T3 and of total thyroxine (T4) in pregnant mothers and in pubertal rats. Testes were studied using light microscopy at 18 and 21 days post coitum or during puberty (21, 35 and 50 days after birth); serum levels of gonadotrophins were also evaluated in pubertal rats. Hypothyroidism had no effect on testicular development during fetal life and when induced in newborn rats it was associated at puberty with reduced serum levels of FSH and LH and with delayed maturation of the testis compared with control rats. The delay in maturation consisted of a reduction in the diameter of seminiferous tubules, and a reduction in the number of germ cells per tubule; this was associated with increased degeneration and arrested maturation of germ cells. In addition, Sertoli cells demonstrated retarded development, as indicated by a delay in the appearance of cytoplasmic lipids and in the development of a tubule lumen. Hormonal and morphological abnormalities were absent in rats treated with MMI plus l-T3. In conclusion, hypothyroidism occurring soon after birth caused reduced levels of gonadotrophins in the serum and a delay in pubertal spermatogenesis, possibly due to retarded differentiation of the Sertoli cells.
Journal of Endocrinology (1991) 129, 35–42
Insulin-like growth factor-binding proteins in tissue fluids from the lamb
Authors: Lord A. P. D. , Martin A. A. , Walton P. E. , Ballard F. J. , Read L. C. 
Published: December 2008

ABSTRACT
Heparinized samples of plasma, cerebrospinal fluid (CSF) and lymph from intestinal, prescapular and popliteal lymph nodes were collected from young lambs in order to characterize and compare the insulin-like growth factor-binding proteins (IGFBPs) in extracellular fluids with those from the circulation. Prior to collection and analysis, the superiority of heparin for plasma preparation was established over EDTA and citrate or the use of serum, according to the extent of IGF-I and IGF-II binding achieved in the high molecular mass IGFBP region in vitro. The IGFBPs were characterized by ligand blotting and competitive binding techniques using radiolabelled IGF-I, IGF-II and the truncated IGF analogue, des(1–3)IGF-I, as well as by ligand blotting of fractions after Superose 6 chromatography of incubations of fluids with labelled factors. This combined analysis demonstrated an IGF-II-specific binding protein at approximately 250 kDa that was present in plasma and each lymph type and presumably represented the soluble type-2 IGF receptor; a complex of 130 kDa containing 52 kDa and 46 kDa binding proteins that was labelled by all three IGF peptides was particularly evident in plasma and intestinal lymph and was probably a complex between IGFBP-3 and the acid-labile subunit; and a group of binding proteins that chromatographed as IGF complexes at approximately 50 kDa. This last group contained IGFBP bands of 52, 46, 35, 28 and 23·5 kDa in plasma and all lymphs as well as an IGF-II-specific band of 22 kDa in prescapular and popliteal lymphs. CSF differed qualitatively from plasma and lymph in that the 52/46 kDa IGFBP bands were undetectable in this fluid; the 35 kDa band was the predominant binding protein, and neither this nor the 28, 23·5 and 22 kDa proteins bound des(1–3)IGF-I to any significant extent. The 52,46 and 28 kDa bands in plasma and lymph did bind this ligand. Immunoblots using antisera against bovine IGFBP-2 showed binding at 35 kDa in all fluids as well as several bands at lower molecular masses. Taken together these results show not only marked differences in the binding protein profiles of sheep plasma, lymph and CSF, but both qualitative and quantitative differences between intestinal, prescapular and popliteal lymphs. We speculate that the differences between lymphs may result from tissuespecific release of binding proteins into extracellular fluid.
Journal of Endocrinology (1991) 129, 59–68
The effect of retinoic acid on parathyroid hormone- and parathyroid hormone-related peptide-induced intracellular calcium in a rat osteosarcoma cell line, UMR106
Authors: Short A. D. , Brown B. L. , Dobson P. R. M. 
Published: December 2008

ABSTRACT
We have examined the effects of parathyroid hormone (PTH) and PTH-related peptide (PTH-rP) on intracellular calcium (Ca2+i) in a rat osteogenic sarcoma cell line, UMR106. Synthetic bovine (b)PTH(1–34) caused a small inconsistent rise in Ca2+i in UMR106 cells, whilst cells pretreated with retinoic acid (RA, 1 μmol/l) for 18 h exhibited reproducible, significant and dose-dependent increases in Ca2+i levels in response to bPTH. The effect of RA on PTH-induced changes in Ca2+i were dependent upon both dose and time. Purified human (h)PTH-rP(1–34) increased Ca2+i in the absence of RA in the same cells. However, RA increased the magnitude of PTH-rP-stimulated changes in Ca2+i without affecting the concentration required for a maximal response. RA also prolonged the delay before the Ca2+i response was observed. Maximal responses to PTH-rP were greater in magnitude than those to PTH. These changes appeared not to be due to cyclic AMP (cAMP), since neither dibutyryl cAMP (1 mmol/l) nor forskolin (15 μmol/l) affected Ca2+i. PTH- and PTH-rP-mediated Ca2+i transients were not completely abolished by the absence of extracellular calcium, and both peptides increased basal levels of inositol trisphosphate. PTH and PTH-rP were subject to mutual desensitization, but were not desensitized by prostaglandin E2. PTH(7–34) antagonized PTH- but not PTH-rP-mediated Ca2+i transients. We conclude that there may be some important differences in the mechanism of action of PTH and PTH-rP.
Journal of Endocrinology (1991) 129, 75–81
Corticotrophin-releasing factor-41, vasopressin and oxytocin release into hypophysial portal blood in the rat: effects of electrical stimulation of the hypothalamus, amygdala and hippocampus
Authors: Tannahill L. A. , Sheward W. J. , Robinson I. C. A. F. , Fink G. 
Published: December 2008

ABSTRACT
The role of the paraventricular nuclei (PVN), amygdala and hippocampus in the control of the hypothalamic-pituitary-adrenal axis has been studied by determining the effect of electrical stimulation of the PVN, amygdala and hippocampus on the release of corticotrophin-releasing hormone (CRF-41) and arginine vasopressin (AVP) into hypophysial portal blood and ACTH and corticosterone into peripheral blood. Adult female Wistar rats were anaesthetized with sodium pentobarbitone and stimulation was carried out through previously implanted bipolar, glass-insulated platinum electrodes. Hypophysial portal blood was collected 30 min before and 30 min during the application of the stimulus which consisted of trains (30 s on and 30 s off) of biphasic rectangular pulses with a frequency of 50 Hz, pulse width 1 ms and amplitude 1 mA. Bilateral stimulation of the PVN increased while unilateral stimulation of the amygdala decreased the release of CRF-41 into hypophysial portal blood. The threefold increase in release of CRF-41 induced by PVN stimulation correlated with a marked increase in peripheral plasma concentrations of ACTH and corticosterone. Stimulation of the hippocampus had no significant effect on CRF-41 release, and stimulation of each of the three brain regions had no effect on AVP release into portal blood. These findings were extended in a second study to compare the effects of unilateral bipolar electrical stimulation of the PVN and of the supraoptic nucleus (SON) on the release of CRF-41, AVP and oxytocin. This study was carried out on adult male rats, anaesthetized with sodium pentobarbitone, in which the stimulus was applied through previously implanted concentric stainless-steel electrodes. Unilateral stimulation of the PVN resulted in a significant increase in the release of CRF-41 and a massive increase in oxytocin release into portal blood. Increased release of oxytocin also occurred after unilateral stimulation of the SON, but CRF-41 secretion was unaffected. The secretion of AVP was unaffected by electrical stimulation of either the SON or PVN. These results (i) provide the first direct proof for the fact that the PVN is the major source of CRF-41 in hypophysial portal blood, and (ii) suggest that the release of CRF-41 may be inhibited by the amygdala.
Journal of Endocrinology (1991) 129, 99–107
Effects of photoperiod on lactotrophs and on dopaminergic and 5-hydroxytryptaminergic neurones in bull calves
Authors: Zinn S. A. , Chapin L. T. , Lookingland K. J. , Moore K. E. , Tucker H. A. 
Published: December 2008

ABSTRACT
This study was conducted to determine whether photoperiod-induced changes in serum concentrations of prolactin in cattle were associated with changes in activity of dopamine or 5-hydroxytryptamine (5-HT) neurones in the infundibulum/pituitary stalk and the secretion rate and number of lactotrophs in the anterior pituitary gland.
Sixteen prepubertal bull calves (approximately 8 weeks of age) were divided into two groups. One group of eight was maintained on a photoperiod of 8 h light : 16 h darkness (8L : 16D) and the other group was exposed to 16L : 8D for 4 weeks. At this time calves were injected with a decarboxylase inhibitor (m-hydroxybenzylhydrazine dihydrochloride, NSD 1015) which blocks the conversion of dihydroxyphenylalanine (DOPA) to dopamine and of 5-hydroxytryptophan (5-HTP) to 5-HT. Calves were killed with pentobarbital 15 min later. Accumulations of DOPA and 5-HTP in selected brain regions were used as indices of activity of dopamine and 5-HT neurones respectively. Secretory rate and number of prolactinsecreting lactotrophs were determined by reverse haemolytic plaque assay.
Relative to calves exposed to 8L : 16D, exposure to 16L : 8D increased serum concentrations of prolactin by eightfold, anterior pituitary gland weight by 23%, release of prolactin from pituitary explants by 57% and the area of the plaque for prolactin-secreting lactotrophs by 70%. There was no difference in the rates of accumulation of DOPA and 5-HTP in the infundibulum/pituitary stalk of animals exposed to 4 weeks of 16L : 8D or 8L : 16D.
It was concluded that increased serum concentrations of prolactin in bulls exposed to a photoperiod of 16L : 8D for 4 weeks were associated with increased secretion of prolactin from lactotrophs which was not the result of a coincident reduction in activity of dopamine neurones or an activation of 5-HT neurones that terminate in the infundibulum/pituitary stalk.
Journal of Endocrinology (1991) 129, 141–148
The self-priming action of LHRH is under negative FSH control through a factor released by the ovary: observations in female rats in vivo
Authors: Koppenaal D. W. , Tijssen A. M. I. , van Dieten J. A. M. J. , de Koning J. 
Published: December 2008

ABSTRACT
Female rats were treated with Metrodin (highly purified urinary FSH from menopausal women) or saline during the oestrous cycle. On the day of pro-oestrus they were anaesthesized with phenobarbital and received four repetitive LHRH injections 1 h apart. This treatment with FSH suppressed the unprimed LH response to the first LHRH injection. During the subsequent injections the maximal LHRH self-priming was delayed by 3 h till the fourth LHRH stimulation. At this time, LH release in response to LHRH was equally as high as shown in the saline controls after the second LHRH injection. Ovariectomized rats did not show the self-priming effect and FSH treatment was ineffective in suppressing LHRH-induced LH release. Administration of FSH followed by an additional 4- or 24-h period before LHRH stimulation were equally effective in suppressing the unprimed LH release and delaying (up to 3 h) the maximal priming of LH release by LHRH. Even 4–20-fold increased amounts of LHRH did not affect the suppressed unprimed release of LH after FSH treatment. Treatment with FSH did not change oestradiol and progesterone levels.
It was concluded that FSH treatment suppresses the unprimed LHRH-induced LH release and delays maximal LHRH self-priming by enhancing the release of an ovarian factor.
Journal of Endocrinology (1991) 129, 205–211
Glucocorticoid-induced hypertension in rats: role of the central muscarinic cholinergic system
Authors: Torres N. , Fanelli M. , Alvarez A. L. , Santajuliana D. , Finkielman S. , Pirola C. J. 
Published: December 2008

ABSTRACT
Betamethasone was administered on alternate days to rats, and the role of the central cholinergic system in the development of hypertension assessed. After 15 days of treatment the systolic blood pressure of treated rats was significantly higher than that of control rats. Peripheral administration of atropine but not of methyl atropine reduced systolic pressure in glucocorticoid-treated rats and had no effect in controls. Therefore, [3H]quinuclidinyl benzylate binding, sodium-dependent high-affinity choline uptake and choline acetyltransferase studies were performed in the septal area, anteroventrolateral medulla (AVLM), anterior hypothalamic preoptic area (AH/PO) and hypothalamus. The density of muscarinic receptors was increased in the hypothalamus and AVLM of treated rats without significant changes in affinity. Choline acetyltransferase activity significantly decreased in the AVLM and increased in the AH/PO. In addition, a decrease in the hypothalamus and an increase in the AH/PO of sodium-dependent high-affinity choline uptake was observed in glucocorticoid-treated rats. These results suggest the presence of an enhanced muscarinic cholinergic activity in several brain nuclei in rats with glucocorticoid-induced hypertension. This activation could be due to pre- and post-synaptic hypersensitivity.
Journal of Endocrinology (1991) 129, 269–274
Increase in the concentration of immunoreactive endothelin in human pregnancy
Authors: Iwata I. , Takagi T. , Yamaji K. , Tanizawa O. 
Published: December 2008

ABSTRACT
Maternal plasma concentrations of immunoreactive endothelin (ir-ET) during pregnancy, labour and after birth were measured by radioimmunoassay. Concentrations of ir-ET in the umbilical artery, umbilical vein, amniotic fluid and neonatal urine were also examined.
The mean (± s.e.m.) plasma ir-ET concentration in early pregnancy (4–7 weeks) was 13·7±0·5 pmol/l, which was significantly higher than that in non-pregnant women (5·9±0·3 pmol/l). During pregnancy, plasma ir-ET concentrations gradually decreased to a minimum of 11·5±0·4 pmol/l in weeks 20–23, and then increased again towards term (12·5±0·4 pmol/l after 36 weeks of pregnancy). In women undergoing vaginal delivery, the mean plasma ir-ET concentration (17·1±0·7 pmol/l) increased significantly, compared with that in late pregnancy. After delivery, the plasma ir-ET concentration decreased abruptly to 4·0±0·2 pmol/l on the first day.
Plasma ir-ET concentrations in umbilical vessels were significantly higher than those in maternal plasma. In addition, concentrations in the umbilical artery were significantly higher than those in the umbilical vein in cases of vaginal delivery.
Concentrations of ir-ET in amniotic fluid were much higher than those in maternal or fetal plasma. ir-ET concentrations in neonatal urine on day 1 after birth were below the detection limit (< 0·1 pmol/l) by radioimmunoassay in 70% of the cases examined but on day 5 after birth ir-ET was present at measurable concentrations in all cases.
It is suggested that endothelin may act as a circulating hormone during pregnancy and labour in both maternal and fetal circulations.
Journal of Endocrinology (1991) 129, 301–307
Ontogeny of corticotrophin-releasing factor (CRF) in the ovine fetal hypothalamus: use of multiple CRF antibodies
Authors: Watabe T. , Levidiotis M. L. , Oldfield B. , Wintour E. M. 
Published: December 2008

ABSTRACT
In previous studies, using one particular antibody, immunohistochemical localization of corticotrophin-releasing factor (CRF) in ovine fetal brain was not possible before 90 days of gestation (term is approximately 150 days), although radioimmunoassay of hypothalamic extracts, using a different antibody, had shown CRF to be present from 63 days. The purpose of this study was to use a variety of CRF antibodies in both immunohistochemistry and radioimmunoassay to determine the presence and concentration of the CRF peptide as early in gestation as possible, and to determine whether more than one molecular size of CRF is detectable at any time in gestation. Seven different antibodies were used on hypothalamic tissue or extracts from seven adult sheep and 37 fetuses from 48 to 140 days of gestation. With one ovine CRF antibody (provided by Dr W. Vale, Salk Institute) immunohistochemical detection of CRF-labelled neurones and nerve fibres of the paraventricular nucleus and median eminence was possible from 49 days. The antibody with the greatest sensitivity in radioimmunoassay was one raised against human CRF, Ab-code R1 (provided by Dr E. Hillhouse, University of Newcastle upon Tyne). The hypothalamic contents of CRF (ng/whole hypothalamus) were 0·28±0·06 (mean ± s.e.m.) (n = 4), 9·0±0·6 (n = 5), 14·3±0·6 (n = 5), 30·0±3·4 (n = 4) in fetuses at 48–50, 100–109 and 139–140 days of gestation and in adult sheep respectively. At all ages only one peak of CRF-like activity, which co-eluted with synthetic ovine CRF, was observed after chromatography of hypothalamic extracts, and assays performed with three different antibodies. Thus there are small amounts of CRF in the ovine fetal pituitary from very early in gestation (50 days), and there is no evidence for a larger molecular weight form, as seen in the immature human fetus.
Journal of Endocrinology (1991) 129, 335–341
Effects of administration of testosterone and gonadotrophin-releasing hormone (GnRH) antagonist on basal and GnRH-stimulated gonadotrophin secretion in orchidectomized monkeys
Authors: Khurshid S. , Weinbauer G. F. , Nieschlag E. 
Published: December 2008

ABSTRACT
The aim of the present investigation was to investigate the effects of testosterone on basal and gonadotrophin-releasing hormone (GnRH)-stimulated gonadotrophin secretion in the presence and absence of a GnRH antagonist in a non-human primate model (Macaca fascicularis). Orchidectomized animals were used in order to avoid interference by testicular products other than testosterone involved in gonadotrophin feedback. Concomitant and delayed administration of testosterone at doses that provided serum levels either within the intact range (study 1) or markedly above that range (study 2) did not influence the suppression of basal gonadotrophin release induced by the GnRH antagonist during a 15-day period. To assess the possible effects of testosterone treatment at the pituitary level (study 3) GnRH stimulation tests (500 μg) were performed before and on days 8 and 15 of treatment with high-dose testosterone and GnRH antagonist alone or in combination. Testosterone alone abolished the gonadotrophin responses to exogenous GnRH observed under pretreatment conditions. With GnRH antagonist alone, an increased responsiveness (P <0·05) to GnRH was seen on day 8 and a similar response compared with pretreatment on day 15. Following combined treatment with GnRH antagonist and testosterone, GnRH-induced gonadotrophin secretion was consistently lower compared with that after GnRH antagonist alone (P <0·05), but was increased compared with that after testosterone alone (P<0·05). Thus, in the presence of a GnRH antagonist the feedback action of testosterone on LH and FSH was diminished. The present work in GnRH antagonist-treated orchidectomized monkeys demonstrates that (I) unlike in rats, testosterone fails to stimulate FSH secretion selectively, (II) the negative feedback action of testosterone on GnRH-stimulated LH and FSH secretion is altered in the presence of a GnRH antagonist and (III) GnRH antagonists induce a transient period of increased responsiveness of gonadotrophic hormone release to exogenous GnRH. The observation that a GnRH antagonist reduced the feedback effects of testosterone suggests that testosterone action on pituitary gonadotrophin release, at least in part, is mediated via hypothalamic GnRH.
Journal of Endocrinology (1991) 129, 363–370