bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pulsatile prolactin secretory patterns throughout the oestrous cycle in the rat
Authors: Lafuente A. , Marcó J. , Esquifino A. I. 
Published: December 2008

ABSTRACT
Prolactin secretion throughout the oestrous cycle in the rat remains at a low level and fairly constant, with the exception of the surge at pro-oestrus. The present study was designed to characterize possible changes in pulsatile patterns of prolactin during the oestrous cycle of the adult female rat. Mean values of prolactin increased from dioestrus-2 to pro-oestrus and then decreased to the values found at dioestrus-1. The number of peaks remained fairly constant in any phase of the oestrous cycle. The absolute amplitude of the peaks increased numerically but was not statistically significant from dioestrus-2 to pro-oestrus then decreasing until dioestrus-1. No changes in the relative amplitude or duration of the peaks throughout the oestrous cycle were detected. The results indicated that there is a similar pulsatile pattern of prolactin at any stage of the oestrous cycle, when samples were obtained during the morning.
Journal of Endocrinology (1993) 137, 43–47
Isolation of FSH from bovine pituitary glands
Authors: Wu J.-B. , Stanton P. G. , Robertson D. M. , Hearn M. T. W. 
Published: December 2008

ABSTRACT
An improved method is described for the isolation of FSH from bovine pituitary glands. The purification procedure consisted of an initial ammonium sulphate precipitation step followed by triazine-dye chromatography, immobilized metal affinity chromatography, high-performance anion-exchange chromatography and gel filtration. Three highly purified bovine FSH preparations (designated bFSH-A, -B and -C) were obtained, giving yields of approximately 5·7 mg FSH/kg bovine pituitary glands (wet weight), with specific radioreceptor activities for bFSH-A, -B and -C of 61, 25 and 29 units (NIH-FSH-S1)/mg protein respectively. The corresponding biological activities were 217 (bFSH-A), 62 (bFSH-B) and 86 (bFSH-C) units/mg, as measured by an FSH in-vitro bioassay. LH levels were found to be < 1% (w/w) as determined by an LH in-vitro bioassay.
SDS-PAGE of these bFSH preparations under reducing conditions in 16% polyacrylamide gels showed two major silver-staining bands of apparent molecular masses 19·5 kDa and 15·8 kDa. Their amino acid compositions were in close agreement with the expected composition, based on the bFSH cDNA sequence and results reported by other investigators. N-terminal sequencing of the bFSH-A preparation yielded two major sequences consistent with α- and β-subunits, and a third minor (< 20%) sequence consistent with the α-subunit clipped at amino acid residue 6. It was concluded that the bFSH purification procedure reported here is a rapid method which produces bFSH in high yield and high purity, with radioreceptor and in-vitro specific activities comparable with those previously reported by other investigators.
Journal of Endocrinology (1993) 137, 59–68
Effects of FSH and testosterone on intratesticular insulin-like growth factor-I and specific germ cell populations in rats treated with gonadotrophin-releasing hormone antagonist
Authors: Spiteri-Grech J. , Weinbauer G. F. , Bolze P. , Chandolia R. K. , Bartlett J. M. S. , Nieschlag E. 
Published: December 2008

ABSTRACT
Evidence derived predominantly from a series of in-vitro studies indicates that insulin-like growth factor-I (IGF-I) plays an important role as a paracrine and autocrine regulator within the testis. We investigated the effects of FSH substitution on spermatogenesis and testicular IGF-I content in rats treated with gonadotrophin-releasing hormone (GnRH) antagonist (ANT) and injected with ethane dimethane sulphonate (EDS), a Leydig cell toxin. FSH treatment partially prevented the marked decrease in intratesticular IGF-I in rats treated with only GnRH antagonist but not in GnRH antagonist + EDS-treated animals (controls, 191·0 ± 4·5; ANT, 80·1 ± 5·6; ANT + EDS, 81·6 ± 3·4; ANT + EDS + FSH, 86·3 ± 1·4; ANT + FSH, 137·7 + 7·3 (s.e.m.) ng/testis). Correlation analysis of testicular IGF-I content with the number of pachytene spermatocytes and round spermatids per cross-section revealed r values of 0·77 and 0·74 respectively (P < 0·001). We then analysed the same parameters in GnRH antagonist-treated rats which, in addition, received daily injections of the antiandrogen flutamide, in order to investigate the potential role of testosterone, as opposed to other Leydig cell products, in the regulation of spermatogenesis and testicular IGF-I. FSH treatment prevented regression of spermatogenesis in rats treated with GnRH antagonist alone but not in GnRH antagonist-and flutamide-treated rats. Testicular IGF-I content was altered in all treatment groups with the most marked changes observed in animals receiving GnRH antagonist and flutamide (FL) with or without FSH (5 or 10 IU/rat twice a day; FSH5 and FSH10) (ANT + FL, 150·32 ± 7·38; ANT + FL + FSH5, 165·28 ± 5·92; ANT + FL + FSH10, 160·17 ± 11·73 vs 464·51 ± 36·04 ng/testis for controls; P < 0·05). Those animals treated with GnRH antagonist and/or FSH had testicular IGF-I levels which were significantly lower than controls and higher than the three groups receiving flutamide and antagonist. A highly significant correlation was established between intratesticular IGF-I and the number of pachytene, round and elongated spermatids per cross-section (r = 0·8 for all three germ cell types). The data presented here provide direct in-vivo evidence for the importance of Leydig cell–Sertoli cell interactions in regulating testicular IGF-I content and spermatogenesis in the testis.
Journal of Endocrinology (1993) 137, 81–89
Cytokines modulate the sensitivity of human fibroblasts to stimulation with insulin-like growth factor-I (IGF-I) by altering endogenous IGF-binding protein production
Authors: Yateman M. E. , Claffey D. C. , Cwyfan Hughes S. C. , Frost V. J. , Wass J. A. H. , Holly J. M. P. 
Published: December 2008

ABSTRACT
Human dermal fibroblasts produce a number of insulin-like growth factor-binding proteins (IGFBPs) including the main circulating form, IGFBP-3. It has been suggested that the regulation of IGFBP secretion may play a major role in modulating insulin-like growth factor (IGF) bioactivity. We have quantified the effects of two cytokines, transforming growth factor-β1 (TGF-β1) and tumour necrosis factor-α (TNF-α) which have opposing actions on fibroblast IGFBP-3 production, and examined their subsequent role in IGF-I mitogenesis. TGF-β1 caused a dose-dependent increase in IGFBP-3 in serum-free fibroblast-conditioned media. TGF-β1 (1 μg/l) resulted in immunoreactive IGFBP-3 levels reaching 286·5 ± 22·4% of control after 20 h, the increase being confirmed by Western ligand blot. TNF-α caused a dose-dependent decrease in fibroblast IGFBP-3 secretion, 1 μg TNG-α/l reducing IGFBP-3 levels to 32·1 ± 11·% of control. This effect was not due to cytotoxicity and was not cell-density-dependent. Fibroblast proliferation was examined using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetric cytochemical bioassay. The addition of IGF-I resulted in dose-dependent growth stimulation after 48 h, the effective range being 20–100 μg/l. The IGF-I analogue Long-R3-IGF-I which has little affinity for the IGFBPs was approximately 20-fold more potent in this assay, and was unaffected by exogenous IGFBP-3. While the addition of 1 μg TGF-β1/l to increasing doses of IGF-I resulted in a fourfold decrease in mitogenic sensitivity to the IGF-I, no such effect was seen with Long-R3-IGF-I. Conversely, 1 μg TNF-α/l increased fibroblast IGF-I sensitivity five-fold, an effect not observed with the IGF-I analogue. Such data suggest that endogenous IGFBP-3 inhibits IGF-I bioactivity and that the regulation of IGF mitogenesis by TGF-β1 and TNF-α can occur via local IGFBP modulation. This may represent a mechanism by which complex growth signals are co-ordinated in vivo.
Journal of Endocrinology (1993) 137, 151–159
Effects of elevated blood insulin-like growth factor-I (IGF-I) concentration upon IGF-I in bovine mammary secretions during the colostrum phase
Authors: Hadsell D. L. , Baumrucker C. R. , Kensinger R. S. 
Published: December 2008

ABSTRACT
The objectives of these studies were to determine if the concentration of insulin-like growth factor-I (IGF-I) in mammary colostrum secretions could be altered through manipulation of IGF-I concentrations in blood and to compare the temporal changes of IGF-I in mammary secretions to those occurring for IgG1. Milking of 15 pregnant Holstein cows was stopped at 8 weeks prepartum and they were randomly assigned to one of three treatments. A control (C) treatment consisted of feeding the animals 100% of NRC requirements for protein and energy. A second group of cows was fed as the control group and injected with 1·8 μmol bovine GH/day. The third group was fed at 70% of NRC requirements for protein and energy to cause a moderate nutrient restriction (NR). Body weight was measured weekly. Blood was collected by tail venepuncture at 4 h intervals for 24 h. Mammary secretions were collected and pooled among contralateral front and rear quarters (diagonal) for measurement of volume, IGF-I and IgG1 concentrations. Samples were collected at −7, −5, −2, 0 and 1 week postpartum. Cows on the NR treatment failed to gain weight during the dry period compared with C cows (P < 0·05). Blood GH and IGF-I concentrations (P > 0·1) were unaffected by NR treatment. Cows treated with GH had higher (P < 0·01) serum GH and IGF-I levels throughout the entire treatment period, and higher serum IgG1 at 5 and 2 weeks prepartum (P < 0·01). Total mass of IGF-I secreted per diagonal averaged 3·6-fold greater for GH-treated cows during the prepartum period than C and NR cows (P < 0·01). The concentration of IGF-I in mammary secretions was not affected by treatment during the prepartum period, but was 40% greater (P < 0·05) in GH-treated cows than C and NR cows at parturition. Analysis of a selective index comparing IGF-I secretion with that of IgG1 suggested that IGF-I does not enter mammary secretions by passive diffusion from blood.
Journal of Endocrinology (1993) 137, 223–230
Influence of N-methyl-d-aspartate on the reproductive axis of male Syrian hamsters
Authors: Urbanski H. F. , Fahy M. M. , Collins P. M. 
Published: December 2008

ABSTRACT
The influence of excitatory amino acids (EAAs) on reproductive neuroendocrine function was investigated in adult male Syrian hamsters of the LSH/Ss Lak strain. Before the study, the animals were maintained in a sexually regressed condition, under short days (SD) and subsequently were either transferred to long days (LD) or kept under SD, for a further 4 weeks. In the former group, photostimulation produced a predictable elevation in the hypophysial contents and serum concentrations of FSH and LH. This was accompanied by an increase in testicular size, an elevation in serum testosterone levels and an increase in spermatogenic activity; the SD hamsters remained sexually quiescent throughout the study. In contrast, SD hamsters that were given daily injections of the EAA agonist, N-methyl-d,l-aspartate (NMA: 50 mg/kg body weight, s.c.), showed stimulatory responses that were generally even more pronounced than those shown by the LD group. Surprisingly, an identical NMA treatment paradigm failed to cause a similar activation of the reproductive axis in LD hamsters that were given daily afternoon injections of melatonin (25 μg, s.c), even though the inhibitory effect of this melatonin treatment is generally regarded as being comparable with that produced by exposure to SD. Although EAAs can acutely stimulate the neurocircuitry that controls LH-releasing hormone secretion, the present findings suggest that EAAs might also exert a long-term stimulatory action by acting further upstream in the photoneuroendocrine pathway.
Journal of Endocrinology (1993) 137, 247–252
Rapid clearance of insulin-like growth factor (IGF)-binding protein species from blood and an associated fall in circulating IGF-I following partial hepatectomy in the rat
Authors: Phillips I. D. , Arany E. , Strain A. J. , Han V. K. M. , Hill D. J. 
Published: December 2008

ABSTRACT
The presence of insulin-like growth factors (IGFs) in blood is regulated by their association with specific IGF-binding proteins (IGFBPs). In turn, the level of IGFBPs in the blood is likely to depend on a dynamic equilibrium between peptide production and clearance to extravascular tissues or organ-specific degradation. Since circulating IGFBPs may largely derive from liver we have employed partial hepatectomy in the rat to study the clearance rate of endogenous IGFBPs from blood once a major site of production is removed. Adult male rats were partially hepatectomized and serum and the remaining liver removed between 30 min and 7 days after surgery. Ligand blot analysis revealed two major species of IGFBP, of 28–30 kDa and 40–44 kDa in sera from control rats or sham-operated rats respectively. The larger species corresponded in size to rat IGFBP-3, but the smaller form was not recognized by antisera against rat IGFBP-1, bovine IGFBP-2 or human IGFBP-5 following Western immunoblot. Following hepatectomy, the levels of both IGFBP forms in the serum declined within 30 min and were barely detectable after 3 h or 6 h. They began to increase again in serum 24 h following surgery. The reduction in IGFBPs following hepatectomy was not primarily due to degradation by specific proteases in serum. Circulating levels of insulin were increased fivefold 3 h after hepatectomy but subsequently returned to control values. The rise in insulin was accompanied by a significant (P < 0·05) reduction in circulating IGF-I after 3 h which persisted at 24 h. Glucose levels in serum showed a transient but non-significant reduction between 90 min and 6 h after hepatectomy. Total RNA was extracted from remnant liver and subjected to Northern blot hybridization with 32P-labelled cDNAs encoding rat IGFBP-1, -2 or -3. Messenger RNA encoding IGFBP-1 was barely detectable in liver from control or sham-operated animals, but increased within 30 min of partial hepatectomy and peaked at 3 h. It subsequently declined and was again barely detectable after 24 h. No expression of IGFBP-2 or -3 mRNAs was found by Northern blot analysis in the liver of control animals or following partial hepatectomy. These results suggest that both IGF-I and IGFBPs in rat serum decreased rapidly following partial hepatectomy, and that this was due largely to the rapid clearance of the peptide and its binding proteins once the major source of production was removed. A rapid induction of IGFBP-1 in the remaining liver may be unrelated to the circulating IGFBPs since immunoreactive IGFBP-1 was not detected in rat serum.
Journal of Endocrinology (1993) 137, 271–280
The paraventricular nucleus and corticotrophin-releasing hormone are not critical in suppressing pulsatile LH secretion in ovariectomized lactating rats
Authors: Tsukamura H. , Ohkura S. , Coen C. W. , Maeda K.-I. 
Published: December 2008

ABSTRACT
Various types of hypothalamic roof deafferentation (RD) (i.e. large anterior (LARD), large posterior (LPRD), small anterior (SARD) or middle (MRD)), electrolytic lesions of the paraventricular nucleus (PVN) or intracerebroventricular (i.c.v.) injection of α-helical corticotrophin-releasing factor(9–41) (α-helical CRF(9–41)) were performed in ovariectomized lactating rats in order to determine the afferent pathway of the suckling stimulus and whether the PVN and corticotrophin-releasing hormone (CRH) are involved in suppressing pulsatile LH secretion during lactation. Animals were ovariectomized on day 2 of lactation (day 0 = the day of parturition). Deafferentations and electrolytic lesions were made on day 7. On the following day, blood samples were taken via an indwelling atrial cannula every 6 min for 3 h. Pulsatile LH secretion with high frequency and amplitude was present in rats with LARD or LPRD despite the suckling. In rats with MRD, LH pulses with a small amplitude were observed when the cut was on or under the ventral margin of the PVN, but there were few LH pulses when the cut passed through the PVN. Electrolytic lesioning of the PVN, however, did not affect the suppression of pulsatile LH secretion during lactation. In addition, i.c.v. injection of α-helical CRF(9–41) (26·1 nmol/10 μl) into the third ventricle on day 8 of lactation did not reverse the suppression of LH secretion by the suckling stimulus. These results suggest that the pathway associated with this inhibition may be rather diffuse and that the PVN region and CRH are not critical in conveying the inhibitory inputs of the suckling stimulus.
Journal of Endocrinology (1993) 137, 291–297
Dopamine D1 receptor analogues act centrally to stimulate prolactin secretion in ewes
Authors: Curlewis J. D. , Clarke I. J. , McNeilly A. S. 
Published: December 2008

ABSTRACT
It is well known that prolactin secretion is inhibited by dopamine acting via the pituitary dopamine D2 receptor. Dopamine D1 receptor analogues also affect prolactin levels although the mechanisms and physiological significance are poorly understood. The present study of the ewe was undertaken to characterize the effects of the D1 receptor agonist SKF 38393 and antagonist SCH 23390 on prolactin in this species and to determine whether the prolactin response to both drugs requires an intact hypothalamo-pituitary axis. Ovariectomized ewes were injected intravenously with vehicle, 0·2, 2 or 20 mg SKF 38393 (D1 agonist) or SCH 23390 (D1 antagonist). At the 20 mg dose, plasma prolactin concentrations were significantly (P <0·01) increased by each drug and returned within an hour to control levels. When injected directly into the lateral ventricles of the brain (intracerebroventricular (i.c.v.) injection), a 100-fold lower dose of SKF 38393 (0·2 mg; P <0·05) was sufficient to stimulate prolactin secretion. In contrast, i.c.v injection of SCH 23390 (0·02 and 0·2 mg) had no effect on prolactin levels and at no dose was there evidence for suppression of prolactin levels. These results are in accord with earlier studies in the rat which suggested that the D1 agonist stimulated prolactin secretion via a direct effect on central dopamine D1 receptors whereas the
D1 antagonist interacted with the pituitary dopamine D2 receptor to increase prolactin secretion. In a further experiment this hypothesis was tested in hypothalamo-pituitary disconnected ewes which were infused with dopamine (0·5 μg/kg per min) for 3 h. After 2 h of the dopamine infusion, animals were challenged with intravenous injections of the vehicle, 20 mg SKF 38393, 20 mg SCH 23390 or 2 mg domperidone (dopamine D2 antagonist). Infusion of dopamine was followed by a significant (P <0·05) decline in prolactin concentrations so that after 2 h prolactin levels were 40% of the preinfusion value. Following injection of the vehicle, SCH 23390 or SKF 38393, prolactin levels continued to decline for the remainder of the experiment. As expected, injection of domperidone was followed by a significant (P <0·05) increase in prolactin to reach peak levels after 30 min. These results demonstrate that peripheral injections of the dopamine D1 agonist SKF 38393 or antagonist SCH 23390 increase prolactin secretion in the ewe. The prolactin response to either drug requires an intact hypothalamo-pituitary axis indicating that SKF 38393 and SCH 23390 act at some central site(s) which is linked with hypothalamic secretion of prolactin-releasing or -inhibiting factors.
Journal of Endocrinology (1993) 137, 457–464
Transient reduction in trabecular bone formation after discontinuation of administration of oestradiol-17β to ovariectomized rats
Authors: Tobias J. H. , Chambers T. J. 
Published: December 2008

ABSTRACT
While the osteopenia associated with oestrogen deficiency is thought to arise from a relative defect in bone formation with respect to resorption, oestrogen administration itself leads to a decrease, rather than an increase, in bone formation. This decrease in bone formation, which arises from oestrogen's inhibitory effect on bone turnover, presumably masks any underlying tendency of oestrogen treatment towards stimulation of bone formation. To investigate this further, we have examined the early effect of discontinuing the administration of oestradiol-17β (OE2; 40 μg/kg on bone formation indices in ovariectomized 13-week-old rats, before the turnover-induced increase in formation occurs. Histomorphometric indices were assessed at the proximal tibial metaphysis 0, 7, 10, 13 and 16 days following discontinuation of OE2 treatment. Measurements of body weight, uterine weight and longitudinal growth rate confirmed that there were rapid effects of OE2 deficiency on these parameters.
We could detect no significant increase in bone resorption, as measured by osteoclast surface and number, until 16 days after ending treatment with OE2; this was coincidental with a reduction in bone volume. Shorter periods of OE2 deficiency were associated with a marked decrease in bone formation, as assessed by dynamic histomorphometric indices. This inhibition of bone formation was largely due to a reduction in double fluorochrome-labelled trabecular surfaces, which were decreased by approximately 70%. We conclude that ending OE2 administration in ovariectomized rats caused a striking decrease in trabecular bone formation, if such indices are assessed prior to the subsequent turnover-induced increase in formation. This suggests that oestrogen treatment in ovariectomized rats is associated with a stimulatory effect on bone formation, in addition to its recognized anti-resorptive action.
Journal of Endocrinology (1993) 137, 497–503
Response to short photoperiod and spontaneous sexual recrudescence in the lesser mouse lemur: role of olfactory bulb removal
Authors: Perret M. , Schilling A. 
Published: December 2008

ABSTRACT
The body weight and sexual activity of the male lesser mouse lemur, a prosimian primate, undergo cyclic changes that are photoperiod-dependent. Exposure to long daylength (LD; 14 h light/day) led to sustained sexual activity, fully developed testes and high plasma testosterone concentrations (228 ±25 nmol/l, n = 10). After 14 weeks under LD, a marked decrease in testosterone levels occurred. Gonadal regression was completed within 20 weeks under LD without concomitant changes in body weight. Exposure to short daylength (SD; 8 h light/day) reinforced the sexual quiescence and was associated with a high ponderal gain (from 60 to 110 g). However, independent of the date of gonadal arrest, the sexual activity of males spontaneously resumed at a fixed time after exposure to SD. The testes developed, testosterone concentrations increased to 155 nmol/l and the body weight decreased (from 110 to 80 g) within 20 weeks under SD exposure. The timing for refractoriness appeared very similar under inhibitory and stimulatory photoperiods. This is consistent with the hypothesis that the perception of a critical daylength is used to regulate the timing of the following sexual phase through a mechanism involving photorefractoriness.
Contrary to cricetid rodents, a direct response to photoperiodic signals for both body weight and sexual activity were not prevented by olfactory bulb removal in male mouse lemurs. In bulbectomized males (n = 12), sexual activity was stimulated by LD and inhibited by SD. Their plasma testosterone levels, however, significantly differed from those of controls in both photoperiods. Likewise, ponderal cycles remained intact but the fattening phase was delayed and reduced. Finally, whereas the sexual recrudescence of bulbectomized males occurred under SD with a delay of only 2–4 weeks, spontaneous testicular regression under exposure to LD did not appear in our experimental photoperiodic conditions.
Journal of Endocrinology (1993) 137, 511–518