bluuebunny/crossref_metadata_2025_split huggingface dataset:
Receptors for glucagon-like peptide-1(7–36) amide on rat insulinoma-derived cells
Authors: Göke R. , Conlon J. M. 
Published: December 2008

ABSTRACT
Specific binding of 125I-labelled glucagon-like peptide-1(7–36)amide (GLP-1(7–36)amide) to rat insulinoma-derived RINm5F cells was dependent upon time and temperature and was proportional to cell concentration. Binding of radioactivity was inhibited in a concentration-dependent manner by GLP-1(7–36) amide consistent with the presence of a single class of binding site with a dissociation constant (Kd) of 204± 8 pmol/l (mean ± s.e.m.). Binding of the peptide resulted in a dose-dependent increase in cyclic AMP concentrations (half maximal response at 250 ± 20 pmol/l). GLP-1(1–36)amide was approximately 200 times less potent than GLP-1(7–36)amide in inhibiting the binding of 125I-labelled GLP-1(7–36)amide to the cells (Kd of 45±6 nmol/l). Binding sites for GLP-1 (7–36)amide were not present on dispersed enterocytes from porcine small intestine.
J. Endocr. (1988) 116, 357–362
Evidence that angiotensin II is a paracrine agent mediating gonadotrophin-releasing hormone-stimulated inositol phosphate production and prolactin secretion in the rat
Authors: Jones T. H. , Brown B. L. , Dobson P. R. M. 
Published: December 2008

ABSTRACT
Gonadotrophin-releasing hormone (GnRH) stimulated the accumulation of inositol phosphates and prolactin secretion in anterior pituitary cells from young male rats. Saralasin ([Sar1,Ala8]-angiotensin II; a competitive antagonist of angiotensin II) inhibited the increase in both inositol phosphates and prolactin in a dose-dependent manner. Since angiotensin II has been shown to be a potent stimulus for inositol phosphate accumulation and prolactin secretion in the lactotroph, these findings suggest that angiotensin II acts as a paracrine agent, being released from the gonadotroph in response to GnRH and causing the lactotroph to release prolactin through an effect on phosphoinositide metabolism. The ability of GnRH to promote prolactin release was lost in pituitaries from older rats, and the increase in total inositol phosphate accumulation was less. These findings provide evidence of a physiological role for the presence of the renin–angiotensin system within the pituitary gland.
J. Endocr. (1988) 116, 367–371
Modification by pertussis toxin of the responses of bovine anterior pituitary cells to acetylcholine and dopamine: effects on hormone secretion and 86Rb efflux
Authors: Schofield J. G. , Khan A. I. , Wood A. 
Published: December 2008

ABSTRACT
Acetylcholine is known to stimulate the secretion of growth hormone and prolactin and the efflux of 86Rb from bovine anterior pituitary cells: dopamine prevents the stimulation of 86Rb efflux and of prolactin but not growth hormone secretion. The sensitivity of these responses to pertussis toxin has been determined.
Treatment of bovine anterior pituitary cells in primary culture with pertussis toxin (18 h, 100 ng/ml) did not modify the stimulation of prolactin secretion by acetylcholine, but prevented its inhibition by dopamine. In lactotrophs, dopamine but not acetylcholine receptors are therefore coupled to secretion through a pertussis toxin substrate. The stimulation of 86Rb efflux by acetylcholine was also unaffected by pertussis toxin and, again, its inhibition by dopamine was prevented.
Treatment of the cells with pertussis toxin enhanced the secretion of growth hormone in response to acetylcholine. Nitrendepine (1 μmol/l) prevented the cholinergic stimulation of growth hormone but not prolactin secretion from these cells. Acetylcholine increased the cytoplasmic calcium concentration and this rise was enhanced by treatment of the cells with pertussis toxin. Nitrendepine partially inhibited the rise in calcium caused by acetylcholine, and prevented the enhancement of the rise following pertussis toxin treatment.
Cholinergic stimulation of growth hormone therefore depends on calcium entry through nitrendepine-sensitive channels, whereas stimulation of prolactin secretion does not, and in somatotrophs a pertussis toxin substrate may limit calcium entry through these channels. These different sensitivities of somatotrophs and lactotrophs to pertussis toxin and nitrendepine may reflect differences in the properties of the predominant calcium currents in the two cell types.
J. Endocr. (1988) 116, 393–401
Effects of physical endurance training on the plasma renin-angiotensin-aldosterone system in normal man
Authors: Hespel P. , Lijnen P. , Van Hoof R. , Fagard R. , Goossens W. , Lissens W. , Moerman E. , Amery A. 
Published: December 2008

ABSTRACT
The effect of physical endurance training on the plasma renin-angiotensin-aldosterone system was studied in 27 normal sedentary volunteers aged between 20 and 55 years, using a randomized two-period cross-over study design. After 4 months of training (2·5 h/week), peak oxygen uptake and physical working capacity at a heart rate of 130 beats/min were increased by 16% (P<0·01) and 29% (P<0·001) respectively, whereas resting heart rate was decreased by 15% (P<0·001). The plasma noradrenaline concentration and haematocrit were both decreased (P<0·01) after training. For the total group of subjects, the small decreases in plasma renin activity (PRA) and in the plasma concentrations of angiotensin-I, angiotensin-II and aldosterone were not statistically significant. However, the change in PRA during the training period was negatively correlated with the increase in physical working capacity (r=−0·49, P<0·01), suggesting that PRA decreased only in those subjects with the greatest increase in exercise capacity. Also, the change in plasma aldosterone during training was negatively related to the rise in physical working capacity (r=− 0·57, P<0·01). Furthermore, the changes in plasma angiotensin-I (r=0·75), angiotensin-II (r=0·49) and aldosterone (r=0·43) during the training period correlated positively with the change in PRA.
It is concluded that physical endurance training, leading to a substantial gain of physical working capacity, suppresses the plasma renin-angiotensin-aldosterone system in normal man.
J. Endocr. (1988) 116, 443–449
GROWTH HORMONE IS MITOGENIC FOR FETAL MOUSE OSTEOBLASTS BUT NOT FOR UNDIFFERENTIATED BONE CELLS
Authors: Slootweg M.C. , van Buul-Offers S.C. , Herrmann-Erlee M.P.M. , van der Meer J.M. , Duursma S.A. 
Published: December 2008

ABSTRACT
More evidence has recently been obtained indicating that growth hormone (GH) has a direct effect on bone. However, it is not clear which cell type reacts to the hormone. The present study used osteoblast-like cells derived from sequentially digested fetal mouse calvaria. Separately cultured tractions resulted in populations enriched in cells with a more or a less differentiated phenotype. The results showed that GH acts on the cells released last, i.e. those with more characteristics of the osteoblast. In these cells, GH induced strong mitogenic activity. Prolactin was not active.
Re-evaluation of the intratesticular level of testosterone required for quantitative maintenance of spermatogenesis in the rat
Authors: Sharpe R. M. , Donachie K. , Cooper I. 
Published: December 2008

ABSTRACT
The amount of testosterone required for quantitative maintenance of spermatogenesis has been re-evaluated using techniques aimed at minimizing the synthesis of testosterone after removal of the testis. Adult male rats were treated with ethane dimethane-sulphonate (EDS) to destroy the Leydig cells, and were supplemented with 25, 5 or 1 mg testosterone esters by injection every 3 days for 21 days. Serum hormone levels, testicular morphology and spermatogenesis were assessed and the intratesticular levels of testosterone compared in testes either removed under ether anaesthesia and placed in liquid nitrogen (right testis) or removed after collection of blood and placed in ice (left testis). Data for testosterone-supplemented rats were compared with those for control rats and rats treated with EDS alone.
All doses of testosterone suppressed LH and FSH levels in serum to within the hypophysectomized range, and Leydig cell regeneration in EDS-treated rats was prevented completely. Treatment of EDS-injected rats with 25 or 5 mg testosterone maintained testicular weight, the number of germ cells and the diameter of seminiferous tubules at stage VII within or above the control range, although there was a significant increase in the number of degenerating pachytene spermatocytes at stage VII with 5 but not 25 mg testosterone; none of these parameters was maintained at control levels by a dose of 1 mg testosterone.
Levels of testosterone in testosterone-supplemented rats differed little between testes collected in ice and liquid nitrogen, but in controls and rats treated with EDS alone, testosterone levels were overestimated by 75 and 27% respectively when comparing testes collected in ice with those collected in liquid nitrogen. This suggests that synthesis of testosterone does occur after removal and cooling of the testes. Using the data for testes collected in liquid nitrogen, the present results suggest that intratesticular levels of testosterone need to be maintained at 24–46% of control values (i.e. higher than previously shown) for quantitative maintenance of spermatogenesis, although it is argued that even these values probably still represent underestimates.
J. Endocr. (1988) 117, 19–26
Characterization of a plasminogen activator inhibitor induced by glucocorticoids in immature bovine Sertoli cell-enriched cultures
Authors: Coombs R. J. , Jenkins N. 
Published: December 2008

ABSTRACT
Plasminogen activation has been shown to be inhibited by the cell-specific production of a number of protease inhibitors belonging to the serine protease inhibitor family. In the bovine testis this inhibitor production is induced by glucocorticoids. Monospecific antibodies raised against the three known classes of plasminogen activator inhibitor were used to identify which type of inhibitor was secreted by bovine Sertoli cell-enriched cultures. Immunoblot analysis and [35S]methionine labelling of newly synthesized proteins revealed that a novel protein with an apparent molecular weight of 49 kDa, which shares antigenic determinants with placental and macrophage PAI and fibroblast protease nexin, is secreted in response to dexamethasone stimulation. This protein was shown by immuno-adsorption to be a functionally active inhibitor of both tissue-type and urokinase-type plasminogen activators.
J. Endocr. (1988) 117, 69–74
Purification, partial sequences and properties of chicken insulin-like growth factors
Authors: Dawe S. R. , Francis G. L. , McNamara P. J. , Wallace J. C. , Ballard F. J. 
Published: December 2008

ABSTRACT
Insulin-like growth factor-I (IGF-I) and IGF-II have been purified to homogeneity from chicken serum as a step towards the characterization of the roles for these peptides in the growth process. Chicken IGF-I had about half the efficacy of bovine/human IGF-I in a bioassay and in radioimmunoassays with bovine IGF-I as radioligand. Chicken IGF-II competed for the binding of bovine IGF-II to cell receptors while chicken IGF-I reacted minimally in this IGF-II radioreceptor assay. Further evidence of homology was obtained by N-terminal sequence analysis of the first 31 and 35 amino acids of chicken IGF-I and IGF-II respectively. Chicken IGF-I had the same N-terminal as human IGF-I, with the exception of the substitution of serine for asparagine at residue 26. Chicken IGF-II had a unique N-terminal tetrapeptide Tyr-Gly-Thr-Ala, but from residues 5–30 the sequence was identical to that reported for residues 6–31 of human IGF-II. Substitutions also occurred corresponding to residues 32, 33, 35 and 36 of human IGF-II. A variant form of chicken IGF-II that had the same N-terminal pentapeptide as human IGF-II was also detected.
J. Endocr. (1988) 117,173–181
Plasma half-lives of native and modified insulin-like growth factor-I in lambs
Authors: Francis G. L. , McNamara P. J. , Filsell O. H. , Ballard F. J. 
Published: December 2008

ABSTRACT
The clearance of labelled insulin-like growth factor-I (IGF-I) has been measured in lambs following acid gel-permeation chromatography and immunoprecipitation of plasma samples. The half-lives obtained in three experiments were between 5 and 7 h. Chromatography at neutral pH on a Fractogel HW55(S) column demonstrated that all the radioactivity associated with undegraded peptide in plasma was bound to a carrier protein. Similar studies with IGF-I that had been reduced by prior dithiothreitol treatment showed that two-thirds of the initial radioactivity in plasma decayed with a much shorter half-life and represented material that did not bind to carrier proteins in plasma. The remaining radioactivity was both associated with a binding protein and exhibited the characteristically long half-life of the native growth factor. Analysis of plasma samples using reversed-phase chromatography demonstrated that the radioactive component with a long half-life was IGF-I while that with a short half-life had been reoxidized to an incorrect form of the growth factor. When reoxidation of reduced IGF-I was blocked by S-carboxymethylation before injection of the radioactive peptide into lambs, it remained unbound in plasma and had a 0·8–0·9 h half-life. We suggest that reduced IGF-I only associates with the binding protein upon oxidation and correct folding and that this association is necessary in order for IGF-I to have a relatively long half-life.
J. Endocr. (1988) 117, 183–189
Aldosterone secretion and adrenal angiotensin II receptors in the Brattleboro rat
Authors: Laulin J. P. , Simonnet G. , Brudieux R. , Carayon A. , Vincent J. D. 
Published: December 2008

ABSTRACT
The basal secretion of aldosterone, measured in adrenal venous blood, was three- to fourfold lower in Brattleboro than in Long–Evans rats used as controls. Infusion of a low dose of angiotensin II (1 ng/min per 100 g body/wt) to Long–Evans rats caused a fourfold increase in aldosterone release but neither the low dose nor a tenfold higher dose changed the rate of release in Brattleboro rats. Only a very high dose (300 ng/min per 100 g body wt) succeeded in increasing the secretion of aldosterone in Brattleboro rats but throughout the time-course of the infusion, secretion remained about fivefold lower than in Long-Evans rats and the incremental response was reduced by 74·9%. Adrenal zona glomerulosa angiotensin II receptor sites had similar affinity and maximum binding capacity in the two groups of rats. It is suggested that the reduced corticosteroidogenic capacity of the adrenal cortex of Brattleboro rats results from an impairment of the post-receptor mechanisms involved in the biosynthesis of aldosterone.
J. Endocr. (1988) 117, 215–221
Withdrawal of endogenous somatostatin induces secretion of growth hormone-releasing factor in rats
Authors: Miki N. , Ono M. , Shizumen K. 
Published: December 2008

ABSTRACT
Secretion of GH occurs in episodic bursts under the dual control of two hypothalamic peptides, GH-releasing factor (GRF) and GH-inhibiting factor (somatostatin, SRIF). Recent studies in rats suggest that episodic GH secretion is generated by the periodic release of GRF, which is associated with the simultaneous withdrawal of SRIF secretion. To test the possibility that GRF discharge is functionally coupled with the withdrawal of SRIF, we investigated whether acute withdrawal of SRIF can induce GRF release by the rat hypothalamus using highly specific antisera against SRIF and rat GRF. In conscious unrestrained rats, i.v. administration of SRIF antiserum at the period of the GH trough induced a rapid onset of the GH secretory surge with a peak value of 309 ± 67 μg/l (mean ± s.e.m.) 30 min after injection. Pretreatment with antiserum to rat GRF resulted in a ∼83% suppression of the GH surge induced by SRIF antiserum without affecting the trough GH values. GRF antiserum also significantly inhibited the spontaneous GH surge. In urethane-anaesthetized rats, as in conscious rats, an acute phasic GH release was caused by SRIF antiserum despite the interference of anaesthesia with spontaneous GH secretion. A further surge-like GH secretion was not restored during the next several hours, however, with the GH secretory profile being characterized by a tonic increase in the baseline levels of GH. In the anaesthetized rat antiserum to rat GRF, having no effect on basal GH levels, similarly inhibited by ∼66% the acute GH surge induced by SRIF antiserum and decreased by about 30% the later sustained rise in GH.
These results indicate that an acute rather than a chronic withdrawal of SRIF can trigger the phasic discharge of GRF by the hypothalamus, and raise the possibility that SRIF, originally isolated as a hypothalamic hypophysiotrophic GH-inhibiting factor, also acts as a GRF-inhibiting factor within the hypothalamus. We suggest that the episodic GH secretion may be initiated by an acute disinhibition of GRF secretion caused by the sudden withdrawal of SRIF.
J. Endocr. (1988) 117, 245–252
Inhibin secretion by the sheep ovary during the luteal and follicular phases of the oestrous cycle and following stimulation with FSH
Authors: Tsonis C. G. , McNeilly A. S. , Baird D. T. 
Published: December 2008

ABSTRACT
The secretion of oestradiol and inhibin were measured during the follicular and luteal phase of the cycle by a sensitive bioassay using sheep pituitary cells in culture in four ewes in which the left ovary had been autotransplanted to the neck. On day 12 of the cycle, premature luteal regression was induced with an injection of 100 μg cloprostenol (prostaglandin F2α analogue; PG) and ovarian venous blood was collected every 4 h for 72 h. These same four ewes were infused in the ensuing cycle with NIH-oFSH-S14 at 10 μg/h for 48 h immediately after an injection of PG and sampled as above.
During the luteal phase ( − 2 h before PG) both in the control and FSH-infused cycles the inhibin secretion rate (SR) was 27–45 units/min. After PG injection, the inhibin SR declined with time to reach 3·6–5 units/min at the onset of the LH surge (60 h after PG) in the control cycle. In contrast, in the following cycle infusion of FSH after PG injection caused a slight increase in the inhibin SR which then remained raised at 42–50 units/min for up to 60 h after PG. In the late follicular phase the oestradiol SR was greater in the FSH-infused than in the control cycles, indicating multiple follicular development. In the FSH-infused cycle the preovulatory surges of LH and FSH were markedly attenuated.
These data demonstrate that (1) inhibin SR is high during the luteal phase suggesting that the sheep corpus luteum secretes inhibin, (2) in the control cycle inhibin SR declines during follicular maturation at a time when oestradiol SR is increasing but FSH levels are decreasing, and (3) exogenously administered FSH stimulates the secretion of inhibin from the ovary during the follicular phase.
J. Endocr. (1988) 117, 283–291
Gonadotrophin-releasing hormone secretion (GnRH) in anoestrous ewes and the induction of GnRH surges by oestrogen
Authors: Clarke I. J. 
Published: December 2008

ABSTRACT
Anoestrous ewes were studied to determine the pattern of secretion of gonadotrophin-releasing hormone (GnRH) in the resting state and following a single i.m. injection of 50 μg oestradiol benzoate. In three out of four untreated ewes, two or three GnRH pulses were observed over a 6-h sampling period. In the fourth sheep the GnRH pulse frequency was higher (six pulses/6 h), but GnRH pulse amplitudes were lower. Following oestrogen treatment, GnRH pulses continued until the occurrence of an LH surge 12 h later. In five out of six sheep sampled during the oestrogen-induced LH surge a marked rise in GnRH secretion was seen. In the sixth ewe a large pulse of GnRH was seen at the start of the LH surge followed by increased GnRH secretion.
It is concluded that GnRH pulse frequency is lower, generally, during anoestrus than during the mating season, and that oestrogen treatment of anoestrous ewes causes a surge in GnRH secretion unlike that seen in similarly treated ovariectomized ewes or the natural cyclic preovulatory changes in GnRH secretion.
J. Endocr. (1988) 117, 355–360
Differential effects of testosterone, 5α-dihydrotestosterone and oestradiol-17β on plasma concentrations of LH in castrated ferrets
Authors: Tang Y. P. , Sisk C. L. 
Published: December 2008

ABSTRACT
The biological activity of testosterone often depends on the conversion of testosterone within the target cell to an androgenic or oestrogenic metabolite. The purpose of this study was to compare the relative ability of testosterone and two of its metabolites, dihydrotestosterone (DHT) and oestradiol, to suppress LH secretion in castrated male ferrets. Castrated ferrets were treated with five different doses of steroid by implanting various numbers of s.c. silicone elastomer capsules packed with either testosterone, DHT or oestradiol. The lowest dose of oestradiol (0·1 mm capsule length/100 g body weight, mean estimated total release rate of 25 ng/day) significantly suppressed plasma concentrations of LH in castrated ferrets. Higher amounts of DHT (2·5 mm capsule length/100 g body weight, mean estimated total release rate of 88 ng/day) were required for a significant reduction in plasma concentrations of LH. Concentrations of LH were also significantly lowered by testosterone when administered at a 2·5 mm capsule length/100 g body weight; however, estimated total release rate was 312 ng/day from these capsules. The fact that oestradiol was more effective than DHT, and that DHT was more effective than testosterone in inhibiting LH secretion in castrated ferrets, suggests that in gonadally intact ferrets, testosterone may be converted to DHT or oestradiol within target cells that mediate steroid negative feedback on LH secretion.
J. Endocr. (1988) 117, 461–466
INTERFERON-α MIMICS EFFECTS OF OVINE TROPHOBLAST PROTEIN 1 ON PROSTAGLANDIN AND PROTEIN SECRETION BY OVINE ENDOMETRIAL CELLS IN VITRO
Authors: Salamonsen L.A. , Stuchbery S.J. , O'Grady C.M. , Godkin J.D. , Findlay J.K. 
Published: December 2008

ABSTRACT
Ovine endometrial cells were isolated from ovariectomized oestrogen and progesterone-treated ewes and maintained in primary culture. In-vitro treatment with human interferon-α2 (Roferon, Hoffman La Roche) (5, 50 IU/ml) or purified ovine trophoblast protein 1 (oTP-1, 30 ng/ml) significantly attenuated PGF2α (25±17, 29±17, 28±9%±SEM of control [no in-vitro treatment = 100%] respectively, N=4 ewes) and PGE (11±4, 16±4, 16±5% of control) release from the cultured cells. Fluorography of two dimensional polyacrylamide gel electrophoretic analyses of proteins secreted by the cells following 35S-methionine incorporation, revealed that synthesis and secretion of the same "pregnancy-related" proteins was stimulated by both interferon-α2 and oTP-1. Thus, interferon-α2 (which has sequence homology with oTP-1) acts on the ovine endometrium, eliciting similar biological responses to those of oTP-1.
Effect of phorbol esters and diacylglycerol on steroid metabolism in isolated rat hepatocytes
Authors: Allan C. J. , Skett P. 
Published: December 2008

ABSTRACT
Hepatocytes, isolated from adult male rats and maintained in serum- and hormone-free medium, were pretreated with phorbol esters known to activate protein kinase C (4β-phorbol-12-myristate-13-acetate) and to be inactive in this respect (4α-phorbol and its 12,13-didecanoate ester). Subsequently the cells were assayed for steroid-metabolizing capacity using androst-4-ene-3,17-dione as substrate. The active phorbol ester was seen to inhibit steroid metabolism markedly after 1 h whereas the inactive derivatives did not show this effect. The endogenous activator of protein kinase C (diacylglycerol) was also seen to inhibit steroid metabolism in a manner similar to the 4β-phorbol ester. Hepatic steroid metabolism is, thus, inhibited by activation of protein kinase C and this may be one of the mechanisms by which the regulatory hormones (e.g. growth hormone) affect steroid metabolism in the liver.
J. Endocr. (1988) 118, 19–23