bluuebunny/crossref_metadata_2025_split huggingface dataset:
Catecholamines and ascorbic acid as stimulators of bovine ovarian oxytocin secretion
Authors: Luck M. R. , Jungclas B. 
Published: December 2008

ABSTRACT
The effects of catecholamines and ascorbic acid on cultured bovine granulosa cells have been examined to assess their possible role in the initiation and maintenance of luteal oxytocin secretion. The actions of these agents have also been compared with the previously reported ability of follicular theca tissue to enhance oxytocin secretion.
Using granulosa cells cultured in serum-supplemented medium, we observed a highly significant enhancement of oxytocin secretion in the presence of adrenaline and noradrenaline, particularly over the concentration range 1–10 μmol/l. This effect was accompanied by smaller and less consistent changes in progesterone secretion and did not involve any change in the time-course of oxytocin secretion. Acetylcholine was without effect. Ascorbic acid stimulated oxytocin secretion when used alone over a range of concentrations, but was also able to synergize with adrenaline. Lactic acid was ineffective. The stimulation of oxytocin secretion by adrenaline could be blocked by equimolar propranolol, but the stimulation of progesterone was not blocked. Propranolol had a variable effect on the ability of theca tissue to stimulate oxytocin secretion by granulosa cells but the results also suggested the presence of some β-agonistic activity in the culture medium.
We conclude, first, that catecholamines may be involved in the regulation of ovarian oxytocin secretion, secondly, that ascorbate may regulate oxytocin secretion through its involvement in the biosynthesis of oxytocin but also through interaction with catecholamines and, thirdly, that the stimulatory action of theca tissue probably does not involve the action of β-agonists.
J. Endocr. (1987) 114, 423–430
Passive immunization of pregnant goats against ovine LH
Authors: Malecki J. , Jenkin G. , Thorburn G. D. 
Published: December 2008

ABSTRACT
Groups of three goats at 50, 90 and 130 days of gestation were passively immunized against ovine LH (oLH) by i.v. infusion of 8 ml serum equivalent of the immunoglobulin fraction of rabbit anti-oLH serum (LHAS). Goats at the same stages of gestation as above served as controls and received 8 ml serum equivalent of the immunoglobulin fraction of normal rabbit serum (NRS). Plasma concentrations of progesterone were determined by specific radioimmunoassay of blood collected at 20-min intervals from 6 h before infusion of LHAS or NRS to 12 h after infusion. Less frequent sampling was performed from 2 days before to 6 days after infusion. Plasma from all LHAS-immunized goats exhibited binding of oLH. Twelve hours after immunization, titres ranged from 1:135 to 1:215. All LHAS-treated goats had titres of less than 1:10 by 5 days after immunization, but a low level of oLH binding was still detectable. Treatment with LHAS or NRS did not shorten the length of gestation, with all goats delivering live offspring between 142 and 147 days after conception. Plasma concentrations of LH ranged from less than 0·15 μg/l to 4·8 μg/l and were greater than 0·15 μg/l in 181 of 255 samples (71%) for both the NRS-treated group, throughout the experiment, and the LHAS-treated groups before infusion of antiserum. Luteinizing hormone was not detectable in plasma samples obtained after LHAS infusion in goats at 50 or 130 days of pregnancy. Plasma concentrations of LH exceeded 0·15 μg/l in only five of 51 (10%) samples in 90-day-pregnant goats treated with LHAS, the maximum value reached being 0·80 μg/l.
Plasma concentrations of progesterone did not alter significantly after infusion of LHAS or NRS at 50, 90 or 130 days of gestation, nor were they significantly different between the groups treated with LHAS and NRS.
The role of LH in the maintenance of pregnancy in the goat after 50 days of gestation is questioned.
J. Endocr. (1987) 114, 413–436
Thyroid hormones regulate the amount of thyrotrophin-releasing hormone in the hypothalamic median eminence of the rat
Authors: Mori M. , Yamada M. 
Published: December 2008

ABSTRACT
The negative-feedback action of thyroid hormones on TRH in the hypothalamic median eminence was examined. Thyroidectomy caused a progressive decrease in TRH content of the median eminence, but not of the whole hypothalamus. In contrast, it did not affect the LHRH content of the median eminence. Administration of thyroid hormone prevented the decrease in TRH content of the median eminence after thyroidectomy. Destruction of the hypothalamic paraventricular nucleus (PVN) led to a significant reduction in TRH content of the median eminence in normal and thyroidectomized rats. These data provide evidence that thyroid hormones regulate directly the amount of median eminence TRH which is derived from the hypothalamic PVN in the rat.
J. Endocr. (1987) 114, 443–448
Comparison of receptors for insulin-like growth factor II from various rat tissues
Authors: Taylor J. E. , Scott C. D. , Baxter R. C. 
Published: December 2008

ABSTRACT
Receptors for insulin-like growth factor II (IGF-II) have been compared in solubilized microsomal membranes from rat lung, brain, kidney, heart, epididymal and subcutaneous fat, ovary, testis and adrenals. Highest binding/μg protein was seen with testicular membranes. Receptors from all tissues showed high affinity for human IGF-II (mean association constant = 65 litres/nmol) and a high degree of specificity (mean IGF-I cross-reactivity 0·3%; no cross-reactivity with insulin). Affinity labelling followed by sodium dodecyl sulphate polyacrylamide gel electrophoresis showed binding was only to a type-II IGF receptor, with a major band seen at a molecular weight of about 230 000 in lung, brain, kidney and testis, and 240 000 in heart, fat and adrenal gland. All tissues showed broad or bimodal pH dependence of binding, with optima seen at about pH 6 and pH 9. Mild stimulation of IGF-II binding by low calcium concentrations (1–2 mmol/l) was seen in all tissues, although higher concentrations were inhibitory in the brain. It was concluded that IGF-II receptors from different rat tissues, when studied under uniform conditions, show similar binding affinities but differences in size and regulation which might be missed if receptors are examined in separate studies.
J. Endocr. (1987) 115, 35–41
Endocrine control of plasma concentrations of calcium-binding protein in the pig
Authors: Maunder E. M. W. , Pillay A. V. , Care A. D. 
Published: December 2008

ABSTRACT
The aetiology of the rise in plasma calbindin-D9k (vitamin D-induced calcium-binding protein; CaBP), following insulin-induced hypoglycaemia, was studied in the pig. ACTH led to a rise in plasma concentrations of both CaBP and cortisol. Metyrapone, which blocks cortisol synthesis, abolished the increases in plasma concentrations of CaBP and cortisol normally observed in response to insulin-induced hypoglycaemia. However, there was no significant rise in plasma concentrations of CaBP in response to pharmacological or physiological doses of cortisol.
Injection of clonidine, an α2-adrenergic agonist, led to a rise in plasma concentrations of CaBP, whereas phenylephrine, an α1-adrenergic agonist, tended to exert an inhibitory effect. Also, administration of phentolamine (an α-adrenergic blocker) before injection of insulin abolished the usual increase in plasma concentrations of CaBP, whereas propranolol (a β-adrenergic blocker) enhanced the normal increase in plasma concentrations of CaBP in response to insulin-induced hypoglycaemia. Isoproterenol, a β-adrenergic agonist, was without effect on plasma CaBP. Neither GH nor glucagon appear to be involved in the rise in plasma CaBP following insulin-induced hypoglycaemia. Although atropine abolished the effect of acute hypoglycaemia on plasma CaBP, carbamylcholine was without effect on plasma CaBP concentration. It is concluded that the increases in plasma CaBP induced by either ACTH or α2-adrenergic stimulation may be interrelated since the administration of ACTH can lead to raised plasma concentrations of catecholamines.
J. Endocr. (1987) 115, 121–128
Maintenance of neonatal rat B cells in glucose-depleted medium: a perifusion study
Authors: Wakabayashi S. , Kagawa S. , Nakao K. , Matsuoka A. 
Published: December 2008

ABSTRACT
Two groups of monolayer cultures of pancreatic cells from the neonatal rat were maintained in glucosedepleted TCM 199 medium, supplemented with 5·5 mmol galactose/l, with or without 0·1 mmol 2-deoxyglucose/1. Another group was kept in medium with 5·5 mmol galactose/l alone, following exposure for 2 days to a medium with 5·5 mmol galactose/1 and 10 μmol iodoacetic acid/l to kill fibroblasts selectively. Each of these monolayers was cultured in a perifusion system for a total of 7 days so that phasic insulin secretion could be compared. On day 0, B cells responded in a monophasic fashion to acute challenge with 16·7 mmol glucose/l whereas, in the presence of 10 μmol forskolin/1 and 1 mmol 3-isobutyl-1-methyl-xanthine/l, the same dose of glucose stimulated a biphasic response of approximately the same magnitude. At a concentration of 10 mmol/l, leucine and 2-ketoisocaproate both produced only minimal increases in the second phase of secretion above the basal level. No response to secretagogues was seen under culture conditions without 2-deoxyglucose. In contrast, addition of 2-deoxyglucose to the galactose-supplemented medium stimulated B cells to secrete insulin in a biphasic fashion in response to a single dose of glucose, and the stimulatory effects of leucine and 2-ketoisocaproate were also remarkably increased. Moreover, when exposed to a linear concentration gradient of glucose, leucine or 2-ketoisocaproate, these B cells responded to secretagogues in a dose-dependent fashion. On the other hand, B cells which had been exposed briefly to iodoacetic acid and then cultured in medium with galactose alone, showed a biphasic response to glucose, leucine and 2-ketoisocaproate; however, quantitative relationships differed. Thus the response (total insulin secreted during a 30-min stimulation) of B cells grown in 2-deoxyglucose to glucose was 610%, to leucine 504% and to 2-ketoisocaproate 810% of that of cells exposed to iodoacetic acid. The present data suggest that cultivation of neonatal B cells in a glucose-depleted medium containing 2-deoxyglucose may cause functional maturation.
J. Endocr. (1987) 115,169–175
Studies of the parathyroid hormone gene in normal subjects, and in subjects with primary hyperparathyroidism and familial benign hypercalcaemia
Authors: Almahroos G. M. , Docherty K. , Fletcher J. A. , Webb T. , Heath D. A. 
Published: December 2008

ABSTRACT
Familial benign hypercalcaemia (FBH) closely resembles primary hyperparathyroidism (PHPT) both clinically and biochemically. Using a cDNA probe for the parathyroid hormone (PTH) gene we have studied restriction fragment length polymorphisms in normal British subjects and have shown them to be similar to those found in previous studies in a German population. The pattern of inheritance of these restriction fragment length polymorphisms in a family with FBH shows that the PTH gene is not involved in the pathogenesis of the condition. Limited studies in PHPT indicate that it is unlikely that a major structural defect or rearrangement is responsible for the sporadic form of the disease.
J. Endocr. (1987) 115, 183–186
A decrease in FSH receptors of granulosa cells during follicular maturation in the domestic hen
Authors: Ritzhaupt L. K. , Bahr J. M. 
Published: December 2008

ABSTRACT
The follicles of the ovary in the domestic hen are arranged in a hierarchy. Responsiveness of the adenylyl cyclase enzyme system of the granulosa cells to FSH decreases as follicles proceed towards ovulation. To test the hypothesis that this decline in FSH responsiveness could be the result of a decrease in FSH receptor numbers, an FSH receptor assay was characterized for chicken granulosa cells and used to measure receptor number and affinity of the largest (F1), third largest (F3) and fifth largest (F5) follicles removed 18 h before ovulation. The numbers of binding sites for F1, F3 and F5 follicles (n = 4) were 0·22 ± 0·05, 0·5 ± 0·14 and 1·22 ± 0·27 pmol hormone bound/mg protein respectively, and were significantly (P < 0·001) different among follicles. The apparent association constants for the F1, F3 and F5 follicles were not different and had a value of 23·4 ± 4·9 litres/nmol (n = 12). Our results indicate that FSH receptor numbers decrease in granulosa cells without a change in affinity as follicles approach ovulation. The decrease in FSH receptor numbers is associated with the reported decline in FSH-stimulated steroidogenesis and adenylyl cyclase activity which occurs during follicular maturation.
J. Endocr. (1987) 115, 303–310
Purification of ovine somatotrophs using a combination of density gradient centrifugation and short-term culture
Authors: Gomm J. J. , Ray K. P. , Wallis M. 
Published: December 2008

ABSTRACT
Freshly dispersed or cultured (18 h) ovine anterior pituitary cells were fractionated on 55% sigmoidal Percoll gradients. This resulted in the separation of two sub-populations of cells at densities of 1·075 g/ml (peak I) and 1·055 g/ml (peak II). Radioimmunoassay of fractions from a gradient on which cells were separated before culture showed the profiles of GH and prolactin to be virtually superimposable. After culture, however, the lactotroph population exhibited an apparent shift in its density profile, the lighter population increasing at the expense of the denser one. Immunocytochemistry of the cells remaining in the denser peak (peak I) showed that it consisted of about 65% somatotrophs which was approximately a three-fold enrichment over the proportion of somatotrophs present in the original cell preparation (24%). Refractionation studies indicated that the change in the density profile of the lactotrophs was due to an actual reduction in their density rather than a loss of viability of the denser sub-population. Secretion data showed the purified somatotrophs to be more responsive than the crude cell preparation to the regulatory factors, GH-releasing hormone and somatostatin. This enriched cell population should prove useful in the detailed study of GH secretion.
J. Endocr. (1987) 115, 395–403
Opioidergic modulation of the oestradiol-induced LH surge in the rat: roles of ovarian steroids
Authors: Lustig R. H. , Pfaff D. W. , Fishman J. 
Published: December 2008

ABSTRACT
Sex steroids convey information on the status of the reproductive system, which the brain is able to integrate to promote ovulation, in the form of the LH surge. The present studies examined the influence of alterations in central opioidergic tone to initiate the LH surge, and the roles of oestradiol and progesterone to effect changes in opioidergic tone, by antagonizing this activity using either naloxone or nalmefene (N-cyclopropylmethyl-6-desoxy-6-methylene-noroxymorphone), a long-acting μ- and κ-opiate antagonist. The timing and amplitude of the LH surge was examined in (1) cyclic rats in pro-oestrus and (2) ovariectomized rats with varying doses of oestradiol supplementation. Plasma was obtained hourly through an indwelling intra-atrial catheter between 13.00 and 19.00 h, and later assayed for LH and oestradiol concentrations by radioimmunoassay.
Rats treated with either nalmefene or progesterone on pro-oestrus demonstrated similar advances in the time of initiation of the LH surge by 1–2 h compared with control rats. The effects of nalmefene and progesterone were evident within 2 and 3–5 h of their administration respectively. Conversely, rats treated with progesterone on dioestrus demonstrated low prooestrous oestradiol levels and abolition of the prooestrous LH surge, but continuous naloxone infusion restored the pro-oestrous LH surge, with raised oestradiol concentrations. In ovariectomized rats without oestradiol supplentation, nalmefene alone was able to increase basal LH levels, but unable to facilitate a spontaneous rise in LH amplitude indicative of an LH surge. Supplementation with low doses of oestradiol was itself ineffective in facilitating a spontaneous rise in LH concentration, but nalmefene co-administration significantly potentiated the ability of low doses of oestradiol to induce augmented LH secretion, in addition to advancing the timing of the spontaneous LH rise. Similarly, progesterone co-administration to ovariectomized, oestradiol-primed rats significantly advanced and augmented LH hypersecretion.
The results of these experiments are consistent with the concept that central opioidergic systems normally restrain the initiation of the LH surge, and that blocking opiate receptors removes this inhibition. They advance the hypothesis that oestradiol, the essential signal for LH surge induction, has, as one consequence of its action, the time-specific inhibition of hypothalamic opioidergic tone in the afternoon, which would otherwise restrain the LH surge-generating mechanism. Finally, the biphasic effect of progesterone on the LH surge appears to be mediated through dichotomous actions on opioidergic tone; in the highoestrogen state, progesterone advances LH surge timing, mimicking the effect of an opiate antagonist, but in the low-oestrogen state, progesterone abolishes the subsequent LH surge, and its effect is negated by an opiate antagonist.
J. Endocr. (1988) 116, 55–69
Androgen metabolism and regulation of rat ventral prostate growth and acid phosphatase during sexual maturation
Authors: Orlowski J. , Bird C. E. , Clark A. F. 
Published: December 2008

ABSTRACT
Androgen metabolism and the regulation of rat ventral prostate cell proliferation and secretory function were examined during sexual maturation. Changes in acid phosphatase (AP) characteristics were measured as a marker of androgen-dependent prostatic secretory function. In immature (21-day-old) rats, total AP activity per cell was low (14.2±1.3 mol p-nitrophenol phosphate hydrolysed/h per mg DNA); it increased threefold as the weight, protein and DNA contents of the prostate increased to adult (65-day) levels. This corresponded with significant (P<0.001) increases in the staining intensities of three of the four bands of secretory AP on isoelectric focusing gels. The extent of inhibition of AP by tartrate decreased at the same time. Secretory AP is known to be relatively tartrate-resistant. The changes in AP activity occurred after prostatic 5α-dihydrotestosterone (5α-DHT) levels increased from 4.6 ± 0.7 pmol/mg DNA (21 days) to reach a peak of 17.6±2.3 pmol/mg DNA at 58 days. Prostatic 5α-DHT concentrations were always higher than testosterone levels. Prostatic 5α-androstane-3α,17β-diol (3α-Adiol) levels were lower than 5α-DHT levels except on day 58 when levels peaked dramatically at 26.2±5.5 pmol/mg DNA. Changes in prostatic 5α-DHT and 3α-Adiol levels corresponded with changes in 5α-reductase and 3α-hydroxysteroid oxidoreductase (3α-HSOR) activities. The oxidative reaction of 3α-HSOR was approximately fourfold higher than the reductive reaction, indicating a preference for the formation of 5α-DHT. The plasma levels of testosterone, 5α-DHT and 3α-Adiol cannot account for their respective prostatic levels, indicating the importance of the steroid-metabolizing enzymes in regulating intracellular androgen levels. Changes in the AP characteristics could be correlated with the androgen status of the prostate.
J. Endocr. (1988) 116,81-90
Effect of hypothyroidism on the in-vivo and in-vitro uptake of sugar by rat thymocytes and on the stimulatory response to 3,5,3′-tri-l-iodothyronine
Authors: Segal J. 
Published: December 2008

ABSTRACT
We have previously demonstrated, both in vivo and in vitro, that 3,5,3′-tri-l-iodothyronine (T3) increases the uptake of the glucose analogue 2-deoxy-d-glucose (2-DG) in rat thymocytes by acting at the level of the plasma membrane. In the present study, the effect of hypothyroidism on the basal uptake of 2-DG by rat thymocytes and their response to T3 was examined.
Rats were rendered hypothyroid by thyroidectomy at 21 days of age, and experiments performed with 31-and 56-day-old animals. Uptake of 2-DG by thymocytes from hypothyroid rats, both in vivo and in vitro, was greater in 31-day-old animals and less in 56-day-old animals than that in euthyroid rats. In both age-groups, hypothyroidism increased cellular responsiveness to T3, shifting the dose–response curve to the left. Similar results were obtained in experiments in which animals were rendered hypothyroid by KClO4. Injection of thyroid hormones into rats treated with KClO4 reversed the effects of hypothyroidism on uptake of [3H]2-DG by thymocytes and their response to T3. From these observations it was concluded that hypothyroidism produces a time-dependent change in basal sugar uptake by rat thymocytes, and increases cellular responsiveness to the effect of T3 at the level of the plasma membrane.
J. Endocr. (1988) 116, 107–114
Further evidence that N-terminal pro-opiomelanocortin peptides are involved in adrenal mitogenesis
Authors: Estivariz F. E. , Carino M. , Lowry P. J. , Jackson S. 
Published: December 2008

ABSTRACT
In order to demonstrate the mitogenic effects of N-terminal pro-opiomelanocortin (N-POMC) peptides on the adrenal glands further, female rats with bilateral adrenal enucleation (hereafter referred to as enucleation) were hypophysectomized 11 days after enucleation and injected twice daily with 5 μg purified human N-POMC(1–28), ACTH(1–24) or 0·9% (w/v) NaCl. On day 14 after enucleation, rats were injected with colchicine and, after killing, their adrenal glands weighed, fixed and mitotic counts in histological sections assessed. Plasma corticosterone was measured fluorometrically. In other experiments, rats 7 days after enucleation were hypophysectomized and implanted with osmotic minipumps delivering 5 μg purified N-POMC(1–28) per day. On day 14 after enucleation, animals were treated as above. Collagenase-dispersed adrenal cells were incubated with purified or synthetic N-POMC(1–28) or synthetic N-POMC (1–36) (1–300 nmol/l) and [3H]thymidine incorporation into DNA was determined. Intact female rats were implanted with osmotic minipumps delivering 8 μg purified or synthetic N-POMC(1–28)/day, 8 μg synthetic N-POMC(1–36)/day or saline alone. Mitotic counts were performed on histological sections.
Both s.c. injection or continuous delivery from minipumps of purified N-POMC(1–28) partially prevented the atrophy of regenerating adrenal glands after hypophysectomy (s.c. injection of N-POMC: 2·29 ± 0·92 mitoses/section compared with 0·52 ± 0·39 for controls; minipump delivery: 5·02 ± 0·97 compared with 0·13 ± 0·05; P < 0·01 for both experiments). ACTH did not augment mitotic activity in enucleated– hypophysectomized rats but significantly increased plasma concentrations of corticosterone in s.c. injection experiments. Adrenal weights were not significantly changed. Both purified and synthetic N-POMC(1–28) increased thymidine incorporation in incubated adrenal cells, the synthetic peptide being less potent than the purified peptide. Whilst synthetic and purified N-POMC(1–28) significantly increased mitotic counts in histological sections of intact adrenal glands after chronic delivery from minipumps, N-POMC(1–36) had no significant effect.
It was concluded that N-POMC(1–28) can partially reverse the adrenal atrophy in enucleated rats after hypophysectomy, whereas ACTH is mitotically inactive in the same situation. The low potency of the synthetic peptides compared with purified N-POMC(1–28) preparations reported in this study could be due to differences in secondary structure.
J. Endocr. (1988) 116, 201–206