bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prepubertal reduction of the ovarian follicle population by combined LH-releasing hormone antagonist treatment and unilateral ovariectomy influences follicle characteristics but not the ovulation rate at first oestrus
Authors: van Cappellen W. A. , van Leeuwen E. C. M. , Kramer P. , Meijs-Roelofs H. M. A. 
Published: December 2008

ABSTRACT
The effect on first ovulation of the massive reduction of the total pool of ovarian follicles during the infantile and late juvenile period was studied in rats. Treatment with an LH-releasing hormone antagonist (LHRH-A) during infancy (5 mg/kg body weight on days 6, 9, 12 and 15 of life) was combined with unilateral ovariectomy performed on either day 15 (early ULO) or 2–5 days before the expected day of first ovulation (late ULO). Rats were killed on the day of first or second oestrus, when blood was collected and the (remaining) ovaries were prepared for differential counting of follicles and corpora lutea. In addition, blood was sampled 8 h after ULO and the ovaries studied histologically in the group of rats which were unilaterally ovariectomized 2–5 days before first ovulation.
The time of first ovulation was not influenced by treatment with LHRH-A, early or late ULO, or a combination of LHRH-A treatment and ULO. Ovulation rate after LHRH-A treatment was decreased, but was still within the normal range in intact rats and in early ULO rats compared with saline-treated controls.
Serum FSH concentrations 8 h after ULO performed 2–5 days before first ovulation were similar in saline- and LHRH-A-treated rats (845 ± 59 and 801 ± 99 (s.e.m.) μg/l respectively) and had increased compared with intact controls (216 ± 15 μg/l).
Treatment with LHRH-A resulted in a reduction of more than 50% in healthy and atretic follicles, and late ULO reduced the number of healthy follicles even further. In saline-treated rats late ULO decreased the rate of atresia, but in LHRH-A-treated rats atresia was not reduced further by (late or early) ULO.
It is concluded that even after massive reduction of the pool of ovarian follicles by early LHRH-A treatment combined with late or early ULO, the timing of the first ovulation was normal and ovulation rates, although somewhat lower in some LHRH-A-treated rats, were within the normal range.
Journal of Endocrinology (1992) 135, 439–446
Catecholamines released from local adrenergic axon terminals are possibly involved in fine tuning of steroid secretion from zona glomerulosa cells: functional and morphological evidence
Authors: Vizi E. S. , Tóth I. E. , Szalay K. Sz. , Windisch K. , Orsó E. , Szabó D. , Vinson G. P. 
Published: December 2008

ABSTRACT
The effect of supramaximal electric field stimulation on [3H]noradrenaline (NA) release and hormone production by rat adrenal capsule-glomerulosa preparations was studied using a microvolume perfusion system. A substantial proportion (about 20%) of nerve endings (varicosities) were observed close to zona glomerulosa cells, and about half of them appeared to be catecholaminergic, as judged by the chromaffin reaction of the synaptic vesicles studied at electron microscopic level. In tissue, preloaded with [3H]NA, the release of NA in response to electrical stimulation was frequency-dependent. Reserpinization, calcium removal or inhibition of Na+ influx by tetrodotoxin completely blocked NA release by field stimulation, indicating that the release resulted from axonal activity and is of vesicular origin. Neither the α2-adrenoceptor agonist xylazine nor the muscarine-receptor agonist oxotremorine affected the stimulation-evoked release of [3H]NA, suggesting that, in contrast with other neurones present in the central nervous system or in the peripheral autonomic nervous system but like those in the median eminence, these axon terminals contained few presynaptic modulatory receptors. The NA (10·20 ± 1·79 (s.e.m.) μg/g, n = 9), adrenaline (24·38 ± 5·50 μg/g, n = 9) and dopamine (0·35 ± 0·09 μg/g, n = 6) contents of the preparations were high, as determined by high-performance liquid chromatography. Our observations that the release and content of NA is high, and that a substantial proportion of catecholaminergic axon terminals lie in close proximity to zona glomerulosa cells (median value of the distance 300 nm) or to smooth muscle cells of the vessels, suggest that NA released from local adrenergic neurones without being presynaptically modulated may play an important role in finetuning both steroid production and/or blood flow through the gland, itself a powerful modulator of the adrenocortical response. This local modulating effect of NA may be especially significant when sympathetic activity is enhanced.
Journal of Endocrinology (1992) 135, 551–561
Evidence for lipopolysaccharide binding in human granulosa-luteal cells
Authors: Sancho-Tello M. , Chen T.-Y. , Clinton T. K. , Lyles R. , Moreno R. F. , Tilzer L. , Imakawa K. , Terranova P. F. 
Published: December 2008

ABSTRACT
We investigated whether human granulosa-luteal (GL) cells exhibited lipopolysaccharide (LPS)-binding protein, and the response of follicular aspirate cells to LPS in vitro. Follicular aspirates taken from a human in-vitro fertilization and gamete intrafallopian-tube transfer programme were subjected to Percoll gradients in order to isolate an enriched population of GL cells. GL cells exhibited specific LPS-binding protein, detected by autoradiography of the cellular lysate on SDS-PAGE after the cells were specifically labelled with a radioiodinated, photoactivable and reducible LPS derivative. LPS binding to the cells was also detected by the appearance of immunofluorescence associated with the cellular membrane when incubated with a fluorescent conjugated LPS receptor antibody. Ninety-four per cent of the cells exhibiting immunofluorescent LPS-binding protein were also positive for the steroidogenic enzyme 3β-hydroxysteroid dehydrogenase, as detected by cytochemistry. In order to detect a response to LPS, the enriched population of GL cells were cultured in vitro in the presence or absence of LPS; after 16 h of culture, tumour necrosis factor-α (TNF) mRNA was detected by reverse transcription-polymerase chain reaction and Southern blot analysis of the amplified cDNA. The expression of TNF mRNA was enhanced when the cells were cultured in the presence of LPS, which also significantly enhanced TNF secretion into the media during the 16-h period. These results reveal that GL cells exhibit LPS-binding protein and thus increased TNF secretion occurs in response to LPS in follicular aspirate cells. The source of ovarian TNF may be leukocytes, macrophages and/or GL cells.
Journal of Endocrinology (1992) 135, 571–578
Inhibition of corticosteroid production by sodium pentobarbitone in rat adrenocortical preparations
Authors: Whitehouse B. J. , Purdy S. J. , Abayasekara D. R. E. 
Published: December 2008

ABSTRACT
It is possible that some of the effects of sodium pentobarbitone on the hypothalamo-pituitary-adrenal axis in the intact animal may be attributable to direct actions on the adrenal cortex. The effects of the barbiturate on steroid production by rat adrenal preparations in vitro have therefore been examined. In zona glomerulosa cells, pentobarbitone inhibited basal steroid production in a dose-related fashion. For aldosterone and corticosterone, the doses required for 50% inhibition of production (IC50) were 1·2 mmol pentobarbitone/l and 3·7 mmol/l respectively. Steroidogenesis was inhibited at lower levels of pentobarbitone in the presence of 1 nmol ACTH/l (IC50 = 0·5 mmol pentobarbitone/l for aldosterone and 2·2 mmol/l for corticosterone). In zona fasciculata/reticularis cells, production of corticosterone was similarly reduced with an IC50 of 2·8 mmol pentobarbitone/l for basal production and 1·3 mmol/l for ACTH-stimulated production. The dose-related increases in corticosterone production produced by ACTH (0·1–1000 pmol/l) or dibutyryl cyclic AMP (0·1–1·0 mmol/l) were also eliminated in the presence of 2 mmol pentobarbitone/l. The effects of pentobarbitone (1–4 mmol/l) on the production of pregnenolone and deoxycorticosterone (DOC) were also studied. In zona fasciculata/reticularis cells, the responses of both pregnenolone and DOC were bell-shaped with increases at 1 mmol pentobarbitone/l, which fell back to control levels at 4 mmol pentobarbitone/l. Stimulation of DOC, accompanied by decreases in aldosterone and corticosterone production, was also seen in zona glomerulosa cells at 1 mmol pentobarbitone/l.
The effect of 1 mmol pentobarbitone/l on the conversion of 22(R)-hydroxycholesterol (5-cholestene-3β,22(R)-diol), pregnenolone, progesterone and DOC to corticosterone and aldosterone by zona glomerulosa preparations was studied. There was a comparable reduction in the conversion of these precursors (2 μmol/l) to aldosterone with yields decreased to 20–30% of those found in the absence of pentobarbitone. The dose required for 50% reduction of the conversion of progesterone (2 μmol/l) to aldosterone was 0·55 mmol pentobarbitone/l and for corticosterone the dose was 1·75 mmol pentobarbitone/l.
The results obtained show that pentobarbitone is an effective inhibitor of corticosteroid biosynthesis in rat adrenal cells, and suggest that its effects are brought about by inhibition of cytochrome P450-mediated hydroxylations.
Journal of Endocrinology (1993) 136, 75–83
β-Endorphin in sows during late pregnancy: effects of cloprostenol and oxytocin on plasma concentrations of β-endorphin in the jugular and uterine veins
Authors: Aurich J. E. , Dobrinski I. , Parvizi N. 
Published: December 2008

ABSTRACT
β-Endorphin was measured in the plasma of pigs during late pregnancy and at different stages of the oestrous cycle. In pregnant animals, β-endorphin secretion from uteroplacental tissues into the maternal circulation and the possible effects of oxytocin and the prostaglandin F2α (PGF2α) analogue cloprostenol on β-endorphin release were determined. Plasma β-endorphin concentrations in pregnant sows were significantly higher than in non-pregnant pigs. However, there were no significant changes in β-endorphin values throughout the oestrous cycle. Because the increase in plasma β-endorphin concentrations had occurred before luteolysis and onset of labour it could not be attributed to the stress of parturition. The surgical intervention of a laparotomy increased β-endorphin release into peripheral plasma. Cloprostenol but not oxytocin caused an immediate increase in plasma β-endorphin concentrations. At parturition, endogenous PGF2α may be involved in the regulation of β-endorphin secretion. Concentrations of β-endorphin in the jugular and uterine vein plasma were not significantly different, and so it would appear that β-endorphin in the plasma of pregnant sows is not of uteroplacental origin. In conclusion, changes in the concentration of β-endorphin in peripheral plasma, associated with pregnancy but not the oestrous cycle, exist in pigs. Hence a physiological function of peripheral opioid peptides in the periparturient sow is feasible.
Journal of Endocrinology (1993) 136, 199–206
Regulation of plasma and tissue levels of insulin-like growth factor-I by nutrition and treatment with growth hormone in sheep
Authors: Hua K. M. , Ord R. , Kirk S. , Li Q. J. , Hodgkinson S. C. , Spencer G. S. G. , Molan P. C. , Bass J. J. 
Published: December 2008

ABSTRACT
Tissue and plasma levels of insulin-like growth factor-I (IGF-I), and relative levels of liver IGF-I RNA, were measured in 6-month-old ewe lambs which were well fed (n = 10) or starved (n = 10) for 5 days. Half of each nutrition group was given daily (09.00 h) injections of human GH (hGH; 0·15 mg/kg body weight per day). Blood was sampled daily from 09.00 to 12.00 h at 15-min intervals through jugular vein catheters and the lambs were slaughtered 24 h after the fifth injection of hGH.
Tissue and plasma IGF-I was extracted using an acid-ethanol-cryo-precipitation technique and estimated by radioimmunoassay. Tissue IGF-I was corrected for retained plasma IGF-I using tissue and blood haemaglobin levels. Liver IGF-I RNA levels were monitored by in-situ hybridization.
Plasma IGF-I (nmol/l) was higher in both the fed group and the fed group given GH treatment. Tissue IGF-I from kidneys (nmol/kg) was also higher (P < 0·001) in the fed group. There was no significant difference in IGF-I concentrations in the muscle biceps femoris or liver between fed and starved lambs. Although GH treatment did not increase IGF-I levels in tissues significantly, IGF-I RNA levels in liver were increased (P = 0·02) in both fed and starved animals. The relative liver IGF-I RNA levels positively correlated with their corresponding tissue IGF-I levels in the fed group and the fed group given GH treatment. The lack of a significant IGF-I response to GH in tissues may be due to either the time at which tissues were sampled after the GH treatment or the dose of GH administered. However, the higher IGF-I concentrations in plasma and kidney from fed compared with starved animals and the positive correlations between liver IGF-I and IGF-I RNA levels suggest that tissue and plasma IGF-I is regulated by nutrition and GH, with nutrition playing a critical role in the regulation of tissue and plasma IGF-I in normal lambs.
Journal of Endocrinology (1993) 136, 217–224
FSH and testosterone, alone or in combination, initiate testicular growth and increase the number of spermatogonia and Sertoli cells in a juvenile non-human primate (Macaca mulatta)
Authors: Arslan M. , Weinbauer G. F. , Schlatt S. , Shahab M. , Nieschlag E. 
Published: December 2008

ABSTRACT
The present study was designed to investigate the relative contributions of FSH and testosterone in the initiation of testicular growth and function in primates. Four groups (n = 4/group) of juvenile rhesus monkeys (Macaca mulatta), 12–18 months old, were treated with vehicle, a highly purified human FSH preparation (hFSH; Fertinorm, 3 IU/kg per day), testosterone (testosterone enanthate, 125 mg/week) or FSH plus testosterone, for a period of 12 weeks. Compared with vehicle treatment, the administration of hormones significantly (P <0·05) increased testicular weight and volume, and the diameter of seminiferous tubules. The number of Sertoli cells per tubule cross-section also increased significantly (P <0·05). Numbers of Ad (dark) spermatogonia (reserve stem cells) were not significantly influenced by any treatment. In contrast, the numbers of Ap (pale) spermatogonia (renewing stem cells) were significantly (P <0·05) stimulated with hFSH and testosterone alone. Following the combined treatment, numbers of Ap spermatogonia were also higher compared with control but this effect did not attain statistical significance. In half of the animals in both testosterone-treated groups, a few prophase I spermatocytes were present. Inhibin concentrations reached adult levels in hFSH-treated groups but remained unaffected by testosterone. Conversely, testosterone failed to influence inhibin levels and, unlike hFSH, increased testicular androgen concentration and epididymal weights. Our observations suggest that hFSH and testosterone alone are capable of initiating testicular growth and gametogenesis in an immature primate. Both hormones probably act via activation of the proliferation of Ap spermatogonia, which are considered to be renewing stem cells within the testis. This study also suggests that androgens might be involved in the morphological differentiation of the immature primate Sertoli cell, whereas the secretory activity of the seminiferous tubule, in terms of peripheral inhibin levels, might be under the influence of FSH.
Journal of Endocrinology (1993) 136, 235–243
Insulin-like growth factor-binding protein-1, glucose tolerance and fetal growth in human pregnancy
Authors: Baldwin S. , Chung T. , Rogers M. , Chard T. , Wang H. S. 
Published: December 2008

ABSTRACT
Two hundred Chinese primigravidae had 50 g 3-h oral glucose tolerance tests (OGTTs) twice in pregnancy; between 20 and 24 weeks and between 30 and 34 weeks of gestation. In 149 women, a single sample was taken for insulin-like growth factor-binding protein-1 (IGFBP-1) measurement 0, 1, 2 or 3 h after the glucose load at both visits; in 55 women IGFBP-1 levels were estimated in all four OGTT samples. Fetal growth was assessed by ultrasound performed at the first and second visit and, if possible, at term, and by anthropometry of the neonate. Cord serum IGFBP-1 was measured in 144 of the babies. Mothers who developed gestational diabetes were excluded.
Maternal levels of IGFBP-1 were inversely related to glucose levels at 0, 1 and 2 h in the third trimester of pregnancy. IGFBP-1 measured at 1 h in an OGTT increased between the second and third trimester. There was an inverse correlation between maternal IGFBP-1 measured in the second trimester and all fetal measurements at that time, and with most neonatal measurements and birthweight. Levels of IGFBP-1 in the third trimester were inversely correlated to neonatal abdominal circumference, skinfold thickness and birthweight. Cord blood IGFBP-1 was inversely related to growth of abdominal circumference. The strongest inverse relationship was between IGFBP-1 and maternal weight. Fasting glucose in the second trimester was positively correlated to fetal subcutaneous fat and growth of abdominal circumference. In the third trimester it was related to fetal abdominal circumference, the growth of abdominal circumference, birthweight and neonatal skinfold thickness. In a multiple regression analysis, both glucose and IGFBP-1 were shown to be determinants of birthweight. It is concluded that IGFBP-1 levels are related to glucose tolerance in pregnancy, and that both IGFBP-1 and glucose have a role in determining birthweight.
Journal of Endocrinology (1993) 136, 319–325
The effect of free fatty acids on the in-vitro binding of testosterone in human plasma
Authors: Diver M. J. 
Published: December 2008

ABSTRACT
The effect of supraphysiological levels of free fatty acids (FFA) on the binding of testosterone to sex-hormone binding globulin (SHBG) and on non-SHBG binding in both male plasma and plasma from pregnant women was studied. Six FFAs were added to plasma as individual acids. No alteration in testosterone binding to SHBG could be demonstrated with any of the FFAs in either male plasma or plasma from pregnant women. When the same plasma was heated to destroy SHBG binding, a highly significant (P <0·01) increase in non-SHBG binding was seen in both male plasma and plasma from pregnant women when the unsaturated FFAs oleic, linoleic and linolenic acids were added. No significant difference was demonstrated with the saturated FFAs, palmitic, stearic and arachidic acids.
Journal of Endocrinology (1993) 136, 327–330
Serum levels of adrenal androgens up to adrenarche in Peruvian children living at sea level and at high altitude
Authors: Goñez C. , Villena A. , Gonzales G. F. 
Published: December 2008

ABSTRACT
Serum levels of adrenal androgens were measured in children of both sexes living at sea level and at high altitude using a cross-sectional design. The levels were compared in relation to age at each altitude (150 m and 3400 m above sea level), and the first significant increase in mean levels compared with values at preceding ages was assessed and defined as adrenarche.
A total of 118 boys and 95 girls aged 6–12 years living at low altitude and 95 boys and 104 girls aged 7–15 years living at high altitude, all of them attending public schools, were studied. Serum dehydroepiandrosterone, dehydroepiandrosterone sulphate and androstenedione were measured by radioimmunoassay and height and weight by standard anthropometric techniques. There were two significant increases in serum levels of adrenal androgens, the first observed in children between 6 and 8 years at sea level, and between 7 and 9 years at high altitude, and the second in children between 10 and 12 years at sea level and between 12 and 15 years at high altitude. Serum adrenal androgen levels increased earlier in children at sea level than at high altitude.
It is concluded that adrenarche occurs later at high altitude than at sea level.
Journal of Endocrinology (1993) 136, 517–523
ENDOTHELIN STIMULATES TESTOSTERONE SECRETION BY RAT LEYDIG CELLS
Authors: Conte D. , Questino P. , Fillo S. , Nordio M. , Isidori A. , Romanelli F. 
Published: December 2008

ABSTRACT
The present study was designed to evaluate the effects of endothelin (ET) on rat testicular steroidogenesis in vitro and the involvement of prostaglandins (PG) and extracellular calcium in its mechanism of action. To this purpose we examined the effects of ET-1 and ET-3 on basal testosterone secretion, the influence of ET-1 on PGE2, release, the interaction of ET-1 and ET-3 with human chorionic gonadotrophin (hCG) and the interference of indomethacin (an inhibitor of cycloxygenase) and nifedipine (a calcium-channel blocker) in purified rat Leydig cells. The data indicate that ET-1 and ET-3 stimulate basal and hCG-induced testosterone production although the effects of ET-3 were less marked. In addition, a concomitant release of PGE2, was observed after exposure to ET-1. A sinergistic interaction between ET-1 and hCG in stimulating testicular steroidogenesis was revealed. Indomethacin was ineffective in modifying ET-1 evoked testosterone output, while in the presence of nifedipine the stimulatory effect of ET-1 was completely abolished. Since it has been shown by others that ET-1 is produced by rat Sertoli cells and specific binding sites are present in Leydig cells, the results of our study indicate that such a peptide may be regarded as a new paracrine factor able to influence steroidogenesis in Leydig cells. The action of ET-1 requires the activity of voltage-operated Ca2+ channels, while PGE2 activation is not essential for its steroidogenic effect.
Norethindrone acetate only partially protects the skeleton of rats treated with the LHRH agonist buserelin from oestrogen-deficiency osteopaenia
Authors: Goulding A. , Gold E. 
Published: December 2008

ABSTRACT
In women with endometriosis there is concern that therapeutic use of LH-releasing hormone (LHRH) analogues, to lower ovarian oestrogen production and control endometrial hyperplasia, leads to unwanted oestrogen-deficiency bone loss. We have developed an animal model of this LHRH-mediated oestrogen-deficiency bone loss in the rat, using buserelin. The aim was to use this model to determine whether the progestogen, norethindrone acetate, could counter oestrogen-deficiency bone loss associated with prolonged treatment with the LHRH agonist buserelin. Four groups of animals which had their bones labelled with 45Ca were studied for 4 weeks: group A, control; group B, buserelin treated; group C, norethindrone acetate treated; group D, norethindrone acetate + buserelin treated. Buserelin was given daily (19·2 pmol/kg body wt); norethindrone was given orally three times / week (1·47 μmol/kg body wt). Bone resorption was monitored by measuring the urinary excretion of hydroxyproline and 45Ca and bone 45Ca content. Buserelin-treated rats developed similarly depressed plasma oestradiol-17β values in the presence and absence of progestogen, and both groups given buserelin had significantly smaller uteri than controls or rats given norethindrone without buserelin. However, norethindrone did not prevent buserelin-mediated increases in bone resorption. At the end of the study total body calcium values (mean ± s.d.) in the four groups were (mg) respectively; 2594 ± 123; 2260 ± 92 (P < 0·001 compared with controls); 2616 ± 221; 2415 ± 130 (P < 0·02 compared with controls). Rats given norethindrone and buserelin in combination had higher values (P < 0·02) than animals given buserelin alone, but significantly less total body calcium than controls (P < 0·02). We conclude that progestogen confers partial, but not complete, protection of the skeleton of buserelin-treated rats from oestrogen-deficiency bone loss.
Journal of Endocrinology (1993) 137, 27–33