bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibition of neonatal rat growth and circulating concentrations of insulin-like growth factor-I using an antiserum to rat growth hormone
Authors: Flint D. J. , Gardner M. J. 
Published: December 2008

ABSTRACT
Treatment of rats for 24 h on day 2, 10 or 20 of age with a specific antiserum to rGH (anti-(rGH)), GH, bromocriptine (CB-154) or prolactin failed to influence body weight gain or serum concentrations of insulin-like growth factor-I (IGF-I). On day 28 of age, however, anti-(rGH) completely inhibited body weight gain and markedly reduced circulating IGF-I concentrations, effects which were completely prevented by exogenous ovine GH (oGH). When administered to control rats on day 28 oGH caused supranormal weight gain and serum IGF-I concentrations. These results suggested that GH does not play a significant role in growth or regulation of serum IGF-I until after day 20 of age.
By contrast, when anti-(rGH) was given for 4 consecutive days beginning on day 2 of life, body weight gain was reduced within 48 h and remained so until at least 28 days of age. Tail length was also significantly reduced. The effect was due to inhibition of GH effects since serum GH concentrations were low and exogenous GH prevented the effect. Inhibition of growth during the first 14 days of life occurred in the absence of any effect on serum IGF-I although by 21 days of age serum IGF-I was considerably lower than in control rats.
The prolonged reduction in growth after treatment has stopped appeared to be due to a cytotoxic effect on the pituitary gland since pituitary weight and GH but not prolactin content were significantly decreased. The data are consistent with the hypothesis that in the neonate GH may be processed in serum so that a proportion of it is not recognized by an antiserum to pituitary GH.
It would appear that inhibition of GH secretion reduces growth rate by at least 30–40% up to 14 days of age, 50% by 21 days of age and completely by 28 days. Effects of GH on growth could not be fully explained by regulation of serum IGF-I concentrations.
Journal of Endocrinology (1989) 122, 79–86
Cross-reaction of eye muscle antibodies with thyroid tissue in thyroid-associated ophthalmopathy
Authors: Weightman D. , Kendall-Taylor P. 
Published: December 2008

ABSTRACT
The nature of the association of ophthalmopathy with autoimmune thyroid disease is not understood. Serum autoantibodies to eye muscle have previously been identified and in this study we have explored the hypothesis that there may be shared antigenic determinants between orbital and thyroid tissues. Sera were obtained from patients in whom eye muscle antibodies (EMAb) had been detected by an enzyme-linked immunosorbent assay (ELISA); the sera were preincubated with membrane preparations of thyroid or eye muscle, hepatic membranes being used as control. Tissue-binding antibodies were removed from serum by centrifugation and the supernatant serum was analysed using an indirect ELISA and by immunoblotting. In the ELISA, all sera gave a positive response for EMAb. In one serum, the binding was entirely non-specific. All sera showed significant neutralization of EMAb by eye muscle. In six sera there was reduction of EMAb after exposure to thyroidal antigens, indicative of cross-reaction. Western blotting confirmed the non-specific nature of the binding in one serum. In five of the remaining nine sera, protein bands were identified which interacted specifically with eye muscle and, in two of these, the same determinants were neutralized by preincubation with thyroid tissue. The Western blots confirmed the findings in the ELISA. The determinants recognized by IgG were variable between patients and no common antigen could be identified.
This study demonstrates that, in some cases of thyroid-associated ophthalmopathy, there is cross-reaction of EMAb with thyroidal antigens, but this is variable and not found in every case. This may explain the association of the disease with autoimmune thyroid disease, at least in some cases.
Journal of Endocrinology (1989) 122, 201–206
Trypsinization of bovine parathyroid cells abolishes Ca2+-regulated parathyroid hormone secretion
Authors: Muff R. , Fischer J. A. 
Published: December 2008

ABSTRACT
The secretion of parathyroid hormone (PTH) is inversely related to the extracellular Ca2+ concentration (Cae2+). To test the hypothesis that a Ca2+ sensor on the surface of parathyroid cells is involved in Ca2+-regulated PTH secretion, limited trypsinization of bovine parathyroid cells was carried out. Treatment with trypsin (1·1–10 mg/ml) inhibited, in a dose-dependent manner, PTH secretion stimulated by lowering Cae2+ from 2·0 to 0·5 mmol/l. In control cells, activation of protein kinase C with 12-O-tetradecanoylphorbol-13-acetate (TPA) enhanced PTH secretion at 2·0 mmol Cae2+/1 but not at 0·5 mmol Cae2+/1. In trypsinized cells, however, TPA enhanced PTH secretion at both 0·5 and 2·0 mmol Cae2+/1. Isoproterenol-stimulated PTH secretion was maintained in trypsinized cells, but reduced cyclic AMP production revealed that some β-adrenergic receptors were destroyed. The cytosolic free Ca2+ concentration (Cai2+), as measured with fura-2, was raised within seconds in response to increasing Cae2+ from 0·5 to 2·0 mmol/l and was then lowered within 1 min to a sustained plateau; the changes were the same in trypsinized and control cells. In conclusion, trypsinization of parathyroid cells abolished Ca2+-regulated PTH secretion without affecting Cai2+.
Journal of Endocrinology (1989) 122, 213–218
The implication of opiates in the glucocorticoid-mediated inhibition of LH secretion in rats
Authors: Belhadj H. , De Besi L. , Bardin C. W. , Thau R. B. 
Published: December 2008

ABSTRACT
The present study was designed to test the effect of acute administration of dexamethasone on the postcastration and gonadotrophin-releasing hormone (GnRH)-induced rise of LH, and to examine whether the inhibitory action of glucocorticoids on LH secretion was mediated by the opioid system. Rats were castrated and injected 10–10·5 h later in a first set of experiments with saline, dexamethasone (250 μg/rat), nalmefene (2 mg/kg body weight) or nalmefene plus dexamethasone. The response to GnRH was tested 11 h after castration (time 0) in all groups. Dexamethasone caused a significant (P< 0·005) decrease in basal serum concentrations of LH, while saline and nalmefene did not induce any change. The administration of dexamethasone preceded by nalmefene increased basal concentrations of LH (1·6 times), with an effect significantly greater than that of dexamethasone (P< 0·001), nalmefene (P<0·05) or saline (P<0·005) alone. GnRH induced a significant (P < 0·001) increase in serum concentrations of LH in all groups. In a second set of experiments, administration of naloxone (2 mg/kg body weight) increased LH levels (P<0·05) and similarly reversed the inhibitory effect of dexamethasone on LH. These results indicate (1) that the inhibiting effect of dexamethasone on the post-castration rise of LH is likely to be exerted at a suprapituitary level, since dexamethasone does not decrease the GnRH stimulated LH response, (2) that opioid antagonists have the ability to reverse the glucocorticoid-inhibiting effect on LH and (3) that dexamethasone can enhance the effect of nalmefene at a time when serum concentrations of testosterone are at very low levels. We conclude, therefore, that dexamethasone regulates LH secretion, at least in part, through the same pathways as testosterone.
Journal of Endocrinology (1989) 121, 451–456
The anterior pituitary content of neuromedin U-like immunoreactivity is altered by thyrotrophin-releasing hormone and thyroid hormone status in the rat
Authors: Domin J. , Steel J. H. , Adolphus N. , Burrin J. M. , Leonhardt U. , Polak J. M. , Bloom S. R. 
Published: December 2008

ABSTRACT
In this study we have examined the effects of TRH, thyroid hormones and dopamine on the rat anterior pituitary content of neuromedin U-like immunoreactivity. Oral administration of TRH (20 mg/100 g per day) to euthyroid animals evoked a fivefold increase in peptide content after 12 days of treatment. This effect was found to be dependent upon circulating levels of thyroid hormone, since administration of TRH to thyroidectomized animals failed to show a similar effect without simultaneous treatment with tri-iodothyronine. The possibility that the TRH-induced increase in anterior lobe neuromedin U content reflected alterations in prolactin secretion or synthetic rate was also examined. Treatment of euthyroid animals with a dopamine agonist and antagonist was, however, without effect. These results demonstrate a unique relationship between TRH and thyroid hormone levels in increasing the anterior lobe content of neuromedin U immunoreactivity.
Journal of Endocrinology (1989) 122, 471–476
Regulation of insulin-like growth factor-I and growth hormone receptor gene expression by diabetes and nutritional state in rat tissues
Authors: Bornfeldt K. E. , Arnqvist H. J. , Enberg B. , Mathews L. S. , Norstedt G. 
Published: December 2008

ABSTRACT
Insulin-like growth factor-I (IGF-I) mRNA and GH receptor mRNA levels were analysed in different tissues from rats made diabetic with streptozotocin, fasted rats and rats fed with a protein-reduced diet. Diabetes decreased IGF-I mRNA levels in liver, heart, diaphragm, kidney and aorta, but not in brain. GH receptor mRNA levels were decreased in heart and diaphragm, but not in liver and kidney. Fasting decreased IGF-I mRNA in all tissues studied except brain, and decreased GH receptor mRNA in liver, heart and diaphragm, but not in kidney. A protein-reduced diet decreased hepatic IGF-I mRNA levels but did not significantly affect other tissues, while GH receptor mRNA levels were reduced in liver and diaphragm. In conclusion, both diabetes and limited nutrition affected IGF-I and GH receptor mRNA in different tissues, but the two mRNAs were not co-ordinately regulated in all tissues studied. While reduced GH receptor gene expression may thus be responsible for decreased IGF-I gene expression in some states and tissues, additional regulatory mechanisms may be of importance.
Journal of Endocrinology (1989) 122, 651–656
Growth hormone-releasing factor-induced growth hormone secretion from perifused rat anterior pituitary cells: lack of influence of glucose concentration, and normal responses in pituitary cells from diabetic animals
Authors: Caldwell G. , Hart G. , Kohner E. M. , Burrin J. M. 
Published: December 2008

ABSTRACT
The mechanism responsible for the suppression of GH secretion in hyperglycaemia and hypoglyceamia in rats has been investigated using perifusion of anterior pituitary cells. When perifused with Krebs-Ringer bicarbonate containing normal (5 mmol/l), high (20 mmol/l) and low (1 mmol/l) concentrations of glucose, the GH responses to GH-releasing factor (GRF) were 85 ± 5, 85·5 ± 5·4 and 89 ± 3·0 (s.e.m.)% respectively compared with the initial response to GRF at 5 mmol/l in each column. The mean GH response to GRF from anterior pituitary cells of normal rats was 6·58 ± 0·88 μg/three pituitaries, which was not statistically different from that of cells from rats with streptozotocin-induced diabetes (5·40 ± 0·68 μg/three pituitaries). It is concluded that GH suppression in diabetic rats and during hypoglycaemia is not mediated by changes in the GH response to GRF.
Journal of Endocrinology (1989) 122, 657–660
Purification, amino acid sequences and assay cross-reactivities of porcine insulin-like growth factor-I and -II
Authors: Francis G. L. , Owens P. C. , McNeil K. A. , Wallace J. C. , Ballard F. J. 
Published: December 2008

ABSTRACT
Porcine insulin-like growth factor-I (IGF-I) and IGF-II have been characterized to help define the roles of these peptides in the growth process. The amino acid sequence of porcine IGF-I was found to be identical to the human and bovine peptides. Porcine IGF-II was more similar to human IGF-II than to forms of this growth factor in other mammalian species, differing only in the replacement of asparagine for serine at residue 36. In a biological assay that measures the stimulation of protein synthesis in rat L6 myoblasts, porcine IGF-I was approximately ninefold more potent than porcine IGF-II or bovine IGF-II, while recombinant human IGF-I and IGF-II had half the potency of the respective natural peptides. Porcine and recombinant human IGF-I showed essentially equal competition for binding in a human IGF-I radioimmunoassay while between 0·6 and 1·5% cross-reactivity was observed with human, bovine or porcine IGF-II. A receptor assay for IGF-II demonstrated similar potencies for the three IGF-II peptides, while the cross-reactivity of recombinant human IGF-I was only 0·05%. Porcine IGF-I exhibited a higher cross-reactivity, presumably due to very slight contamination with IGF-II.
Journal of Endocrinology (1989) 122, 681–687
Radioimmunoassay of inhibin in various mammals
Authors: Hamada T. , Watanabe G. , Kokuho T. , Taya K. , Sasamoto S. , Hasegawa Y. , Miyamoto K. , Igarashi M. 
Published: December 2008

ABSTRACT
A sensitive radioimmunoassay (RIA) for the determination of inhibin in peripheral plasma and tissue homogenates of different species has been developed using antisera to partially purified bovine follicular fluid (bFF) inhibin and 125I-labelled bFF 32 kDa inhibin. Antisera were produced by immunization of rabbits with partially purified bFF inhibin prepared by immunoaffinity chromatography. Increasing doses of a high titre antiserum could neutralize the suppressing effect of bFF, porcine follicular fluid and rat ovarian homogenate on FSH secretion from rat anterior pituitary cells in culture. Sensitivity of the assay was 3·1 ng International Research Standard of porcine inhibin per tube. Parallel inhibition curves were obtained for inhibin preparations from female and male animals of ten species, i.e. cattle, goats, sheep, cats, dogs, monkeys, pigs, horses, rats and man. Inhibin subunits and related proteins cross-reacted minimally with the antiserum used in the study. Plasma concentrations of inhibin in adult male and female rats were measured by the RIA before and at various times after gonadectomy. Inhibin levels in peripheral plasma before gonadectomy were significantly higher in adult female than in adult male rats. Inhibin levels decreased abruptly after gonadectomy in both sexes and they correlated negatively with plasma concentrations of FSH. This inhibin RIA will facilitate studies of the physiology of inhibin in various species of animals.
Journal of Endocrinology (1989) 122, 697–704
Lesion of the subfornical organ affects the haemotensive response to centrally administered relaxin in anaesthetized rats
Authors: Mumford A. D. , Parry L. J. , Summerlee A. J. S. 
Published: December 2008

ABSTRACT
Experiments were performed on anaesthetized, lactating rats to investigate the acute central actions of relaxin on blood pressure and vasopressin release. When compared with saline and control injections of isotonic protein extract, administration of relaxin into either the lateral or dorsal portion of the third ventricle caused a significant and sustained rise in arterial blood pressure. In contrast, relaxin administered to the ventral portion of the third ventricle caused only a short-term rise in blood pressure. Injections of relaxin into the fourth ventricle were without significant effect, suggesting that the central actions of relaxin on blood pressure are mediated by receptors restricted to the diencephalon or mesencephalon. A similar ventricular specificity was noted for the central relaxin-induced stimulation of vasopressin release as judged by concentrations of the hormone in the peripheral plasma. It is unlikely that the stimulation of vasopressin release is wholly responsible for the observed pressor effect observed.
Lesion of the subfornical organ negated the pressor effect to relaxin injected into the dorsal region of the third ventricle, but did not affect the pressor response observed after injection of relaxin into the ventral portion of the third ventricle. These results demonstrate a biphasic action of centrally administered relaxin, with the response to dorsally placed third ventricle relaxin being mediated by the subfornical organ, and the response to ventral injections associated with an unknown structure of the ventral third ventricle wall.
Journal of Endocrinology (1989) 122, 747–755
Effects of growth hormone-releasing hormone on the secretion of islet hormones and on glucose homeostasis in lean and genetically obese-diabetic (ob/ob) mice and normal rats
Authors: Bailey C. J. , Wilkes L. C. , Flatt P. R. , Conlon J. M. , Buchanan K. D. 
Published: December 2008

ABSTRACT
The effect of synthetic human growth hormone-releasing hormone(1–40) (hGHRH-40) on the function of the endocrine pancreas and on glucose homeostasis in lean and genetically obese-diabetic (ob/ob) mice and normal rats has been examined. The addition of 1 μmol hGHRH-40/1 to incubated islets from normal lean mice increased insulin release by 90 and 37% at 5·6 and 16·7 mmol glucose/l respectively. Lower concentrations of hGHRH-40 did not affect insulin release. hGHRH-40 (1 μmol/l) increased pancreatic polypeptide release by 50% at 5·6 mmol glucose/l. A range of concentrations of hGHRH-40 (1 nmol/l–1 μmol/l) reduced glucagon release by 42–73% at 5·6 mmol glucose/l, and by 38–70% at 16·7 mmol glucose/l. Somatostatin release was increased (eightfold) by 1 μmol hGHRH-40/1 at 5·6 mmol glucose/l, but at 1 nmol hGHRH-40/l somatostatin release was reduced (by > 50%). At 16·7 mmol glucose/litre 0·01–1 μmol hGHRH-40/l increased somatostatin release (three- to fourfold), but 1 nmol hGHRH-40/l produced a reduction of 50%. In vivo, administration of hGHRH-40 (50 μg/kg body weight i.p.) to fasted lean and ob/ob mice did not alter basal plasma concentrations of glucose and insulin, or the glucose and insulin responses to a concomitant i.p. glucose challenge. Intravenous injection of hGHRH-40 (20 μg/kg body weight) to anaesthetized rats increased plasma concentrations of insulin in the hepatic portal vein. A lower dose of hGHRH-40 (0·2 μg/kg) was ineffective, and neither dose of hGHRH-40 altered plasma glucose. The results indicate that hGHRH-40 exerts dose-dependent effects on the secretion of islet hormones, but this does not appear to be sufficient to produce measurable effects on plasma glucose homeostasis.
Journal of Endocrinology (1989) 123, 19–24
Sustained exposure of toxically damaged mouse pancreatic islets to high glucose does not increase β-cell dysfunction
Authors: Eizirik D. L. , Sandler S. 
Published: December 2008

ABSTRACT
The aim of this study was to clarify whether prolonged in-vitro exposure of either normal or damaged β cells to a high glucose environment can be toxic to these cells. For this purpose NMRI mice were injected intravenously with a diabetogenic dose of streptozotocin (SZ; 160 mg/kg) or vehicle alone (controls). Their islets were isolated 15 min after the injection and subsequently maintained in culture for 21 days in the presence of 11·1 or 28 mmol glucose/l. After this period, during acute glucose stimulation, the control islets showed a marked increase in their insulin release in response to a high glucose stimulus. In the SZ-exposed islets there was a decrease in DNA and insulin contents, and a deficient insulin secretory response to glucose. However, in the SZ-damaged islets as well as in the control islets, culture with 28 mmol glucose/l compared with 11·1 mmol glucose/l did not impair islet retrieval after culture, islet DNA content or glucose-induced insulin release. Thus, the degree of damage was similar in the SZ-treated islets cultured at the two concentrations of glucose. These results suggest that glucose is not toxic to normal or damaged mouse pancreatic islets over a prolonged period in tissue culture.
Journal of Endocrinology (1989) 123, 47–51
Sexual maturation in starlings raised on long or short days: changes in hypothalamic gonadotrophin-releasing hormone and plasma LH concentrations
Authors: Dawson A. , Goldsmith A. R. 
Published: December 2008

ABSTRACT
Is the extended prepubertal period which occurs in most birds due to a juvenile photorefractoriness analogous to photorefractoriness in adults? Starlings were taken from nest boxes 4 days after hatching and hand-reared on long days or short days. In females on long days, hypothalamic gonadotrophin-releasing hormone (GnRH) content and plasma LH concentration remained low. In intact males on long days, plasma LH remained low and the testes remained small, and in castrated birds, plasma LH also remained low. In females reared on short days, hypothalamic GnRH content began to increase dramatically from 4 weeks of age and plasma LH increased from 6 weeks of age. In intact males on short days, there was a slight increase in plasma LH and testicular size, and in castrated males, plasma LH increased markedly from six weeks of age. All birds on long days moulted into adult plumage, whereas those on short days retained juvenile plumage. The changes in birds reared on short days were similar to those found when photorefractory adult birds are transferred to short days. This adds to the evidence that juvenile photorefractoriness is analogous to photorefractoriness in adults, and therefore that the seasonal termination of photorefractoriness is an annual puberty. However, the responses to short days occur later in birds raised on short days than in older birds transferred to short days, which suggests either that short day-induced changes occur more slowly in young birds, or that birds only respond to short days after a certain age.
Journal of Endocrinology (1989) 123, 189–196