bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pertussis toxin-catalysed ADP-ribosylation of endometrial proteins in sheep
Authors: Flint A. P. F. 
Published: December 2008

ABSTRACT
Membrane fractions prepared from the uterine endometrium of untreated ovariectomized sheep contained a 41 × 103 Mr protein that was [32P]ADP-ribosylated by pertussis toxin in the presence of [32P]NAD. Progestin and progestin plus oestrogen treatment in vivo increased the concentration of this protein 2·7- and 3·6-fold respectively. Endometrial extracts from untreated or progestin-treated sheep also contained proteins of Mr 69 × 103 and 120 × 103 which were ADP-ribosylated in the absence of pertussis toxin; these proteins were not ADP-ribosylated in sheep receiving oestrogen. Incubation of endometrial slices from progestin plus oestrogen-treated sheep with oxytocin in vitro increased phosphoinositide hydrolysis 11-fold. This effect was not altered by prior incubation with pertussis toxin, although toxin treatment reduced by 64% subsequent labelling of the 41 × 103 Mr protein when membrane fractions prepared from pretreated slices were incubated with pertussis toxin and [32P]NAD. Thus the endometrium contains a pertussis toxin-sensitive protein which is induced by steroid treatment, but this protein is not involved in the phosphoinositide response to oxytocin.
J. Endocr. (1988) 117, 403–407
Role of the ovaries in inducing mammogenesis in pregnant pigs
Authors: Buttle H. L. 
Published: December 2008

ABSTRACT
Ovariectomy, but not removal of the corpora lutea, of gilts at mid-pregnancy delayed the onset of lobuloalveolar development in the mammary glands. Lactogenesis at the time of parturition was delayed by both ovariectomy and removal of the corpora lutea.
J. Endocr. (1988) 118,41–45
Secretion of progesterone and prostaglandins by cells of bovine corpora lutea from three stages of the luteal phase
Authors: Rodgers R. J. , Mitchell M. D. , Simpson E. R. 
Published: December 2008

ABSTRACT
The secretion of prostaglandins (PGs) by bovine corpora lutea was investigated. Corpora lutea from the early, early-mid and late-mid stages of the luteal phase were dissociated by collagenase treatment and cultured in monolayer in Dulbecco's modified Eagle's medium containing 10% (v/v) fetal calf serum. Treatment with either LH (100 ng/ml) or dibutyryl cyclic AMP (dbcAMP; 1 mmol/l) had no effect on progesterone secretion by early luteal phase cells but stimulated progesterone secretion two- to fourfold by cells from the latter stages. The secretion rates, per μg cell protein, of 6-keto-PGF1α, PGE2 and PGF2α were substantially greater in cells from the early luteal phase than in those from the latter stages, however, all changes in PG secretion in response to treatments were qualitatively similar between cells from the three stages of the luteal phase. The secretion rate of 6-keto-PGF1α was greater than that of PGE2 or PGF2α and was inhibited by treatment with indomethacin (28 μmol/l) but unaltered by treatment with LH, dbcAMP or butyrate (1 mmol/l). Secretion of PGE2 was inhibited by indomethacin but stimulated two-to threefold by treatment with either dbcAMP or butyrate. Secretion of PGF2α was minimal and not inhibited further by treatment with indomethacin, but was stimulated 10- to 40-fold with dbcAMP. Indomethacin treatment inhibited the stimulatory effect of dbcAMP; butyrate had no effect on PGF2α secretion. Treatment with LH had no effect on any of the PGs measured. In these experiments the secretion of progesterone appeared unrelated to any changes in the secretion of PGs. Thus it would appear that the production of progesterone by bovine luteal cells in culture is not related nor dependent upon the secretion of 6-keto-PGF1α, PGE2 or PGF2α, and that LH/cAMP does not regulate the secretion of PGs since LH had no effect on PG secretion and since the effects of dbcAMP appeared not to be through a cAMP-dependent pathway.
J. Endocr. (1988) 118, 121–126
Thyrotrophin-blocking antibodies in goitrous primary hypothyroidism: detection by a highly sensitive bioassay and determination of site of action
Authors: Atkinson S. , Hardwick M. , Kendall-Taylor P. 
Published: December 2008

ABSTRACT
Using a highly sensitive bioassay technique, the presence of antibodies capable of blocking the stimulation of thyrocyte function by TSH has been investigated in the sera of a group of 50 patients with primary hypothyroidism. TSH-blocking activity was detected in immunoglobulin (IgG) preparations from the sera of 13 patients (26%). All 13 IgG preparations blocked both TSH-stimulated iodide uptake and cyclic AMP generation (Spearman's rank correlation = 0·6, p = 0·02). However, only one IgG preparation blocked dibutyryl cyclic AMP-stimulated iodide uptake.
The presence of TSH-blocking antibody activity was associated with goitrous (ten out of thirteen patients) as well as atrophic (two out of thirteen patients) primary hypothyroidism. Furthermore, TSH-blocking activity was not associated with other thyroid autoantibodies, as thyrotrophin-binding-inhibiting immunoglobulins and anti-TSH antibodies were undetectable in all cases and there was no correlation between TSH-blocking activity and the presence or titre of anti-thyroglobulin or anti-microsomal antibodies.
This study indicates that TSH-blocking antibodies are present in the serum of some patients with primary hypothyroidism and are directed towards a site, presumably adjacent to or contiguous with the TSH receptor, that is not the binding site for TSH. The coexistence of TSH-blocking activity and goitre in the majority of these patients implies that these antibodies, although capable of blocking TSH-stimulated thyroid hormone biosynthesis, do not necessarily inhibit the mitogenic action of TSH in vivo.
J. Endocr. (1988) 118, 141–147
Monolayer cultures of pancreatic islet cells from adult rats: effect of 2-deoxyglucose
Authors: Aoki M. , Kagawa S. , Yamamura T. , Matsuoka A. , Utsunomiya J. 
Published: December 2008

ABSTRACT
Techniques for the monolayer culture of pancreatic islet cells from adult rats and the responsiveness of B cells are described. Whole pancreatic tissue was enzymatically dispersed and then cultured for 30 days in tissue culture medium 199 containing 5·5 mmol glucose/l, with or without 1 mmol 2-deoxyglucose/l. In the absence of 2-deoxyglucose, the responsiveness of B cells diminished to almost zero by day 15 and islets degenerated. In contrast, addition of 2-deoxyglucose to the medium resulted in a selective degeneration of fibroblasts, yielding monolayers that consisted mostly of islet cells. In this stationary system in which monolayers of islet cells were maintained in medium with 2-deoxyglucose, insulin secretion from B cells on days 15 and 30 increased in a dose-dependent fashion in response to increasing concentrations of glucose, leucine and 2-ketoisocaproate. Similarly, when exposed to 16·7 mmol glucose/l, perifused B cells showed a biphasic pattern of insulin secretion on day 15. Addition of 10 μmol forskolin/l and 200 nmol 12-O-tetradecanoyl phorbol13-acetate/l remarkably enhanced this response. Likewise, the response to 10 mmol leucine/l or 10 mmol 2-ketoisocaproate/l was biphasic. These results suggest that these monolayer cultures retain the functional properties of the adult rat pancreas, and may be useful not only as a model for the in-vitro study of B cell function, but also for implantation.
J. Endocr. (1988) 118, 173–178
Somatostatin levels and binding in duodenal mucosa of rabbits with ligation of the pancreatic duct
Authors: Guijarro L. G. , Arilla E. 
Published: December 2008

ABSTRACT
Atrophy of the exocrine pancreas was induced in rabbits by pancreatic duct ligation. Somatostatin concentration and binding in cytosol from rabbit duodenal mucosa were studied after 6 and 14 weeks of pancreatic duct ligation. Somatostatin-like immunoreactivity was significantly increased in the duodenal mucosa in both periods. Scatchard analysis showed a parallel increase in the number of binding sites rather than a change in their affinity. The physiological significance of these findings remains to be clarified.
J. Endocr. (1988) 118, 227–232
Effect of glucose concentrations on functional maturation of monolayer-cultured B cells from the rat pancreas
Authors: Wakabayashi S. , Kagawa S. , Yamashita K. , Matsuoka A. 
Published: December 2008

ABSTRACT
The effect of two concentrations of glucose on the maturation of the response of B cells was studied in pancreatic monolayer cultures of the neonatal rat using a perifusion system. After exposure for the initial 3 days to a medium with 5·5 mmol glucose/l and 10 μmol iodoacetic acid/l (day 3), in order to delete fibroblasts selectively, monolayer cultures were kept for a total of 12 days in medium with either 5·5 or 16·7 mmol glucose/l alone. On day 3, B cells responded in a monophasic fashion, with no significant second phase, to acute challenge with 16·7 mmol glucose/1. 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. In contrast, B cells on day 7 cultured in 5·5 mmol glucose/l showed a biphasic response to glucose, leucine and 2-ketoisocaproate. The magnitude in response to glucose was well preserved at day 15 of culture, whereas the stimulatory effects of leucine and 2-ketoisocaproate decreased to 24–57% of that of B cells on day 7. Moreover, B cells on day 7 cultured in 16·7 mmol glucose/l responded in a biphasic manner to glucose, the response being 65% of that of B cells in 5·5 mmol glucose/l. Additionally, the response to leucine and 2-ketoisocaproate still appeared to be monophasic. At day 15 of culture, however, the response of B cells in 16·7 mmol glucose/l to glucose was 105%, to leucine 245% and to 2-ketoisocaproate 127% of that of B cells in 5·5 mmol glucose/l. In conclusion, these results suggest that cultivation in medium with 5·5 mmol glucose/l could induce precocious development of an adult pattern of insulin secretion compared with that in 16·7 mmol glucose/l and, in addition, that the medium with 16·7 mmol glucose/l is superior for long-term culture to the medium with 5·5 mmol glucose/l.
J. Endocr. (1988) 118, 303–310
A comparison of the dynamics of secretion of human growth hormone and LH pulses
Authors: McIntosh R. P. , McIntosh J. E. A. , Lazarus L. 
Published: December 2008

ABSTRACT
Patterns of hypothalamic stimulation causing pituitary hormone release cannot be studied directly in humans; one possible approach is to make inferences from the nature of the response of the target organ as revealed by patterns of pituitary hormones in blood. Replicated, precise assay of LH in frequently sampled blood of women at differing stages of the menstrual cycle has demonstrated previously that secretion of this hormone is compatible with a model of discrete, instantaneous episodes of LH output, which are assumed to be stimulated by isolated bursts of increased stimulatory hypothalamic gonadotrophin-releasing hormone. However, similarly detailed measurements of the dynamic secretion patterns of GH in women reported here, revealed much slower rates of increase of GH concentrations (median time to maximum concentration 38 min) in comparison with LH (13 min) assayed in the same blood samples. These rise rates of GH were uncorrelated with the final amplitude of the peak and were observably discontinuous in half the peaks. Simultaneous i.v. injection of a bolus of mixed GRF and GnRH produced similar dynamics of pituitary release of GH and LH. Thus differences in patterns of natural release of the two hormones appear to be contributed to by differences in the modes of hypothalamic stimulation. Current understanding of control of GH release in animal models suggests that the slow-rising, frequently discontinuous natural peaks of GH in human blood are likely to be caused by interaction between the withdrawal of inhibitory hypothalamic somatostatin and the increased secretion of stimulatory GRF.
J. Endocr. (1988) 118, 339-345
The role of growth hormone in diabetes mellitus
Authors: Holly J. M. P. , Amiel S. A. , Sandhu R. R. , Rees L. H. , Wass J. A. H. 
Published: December 2008

Summary
The insulin and growth hormone (GH)/insulin-like growth factor-I (IGF-I) axis are two endocrine systems that are interlinked at many levels. GH is one of the glucose counter-regulatory hormones, rising in response to hypoglycaemia, it has both intrinsic hyperglycaemic actions and causes insulin resistance. Both IGF-I and its receptor have high structural and functional homology to insulin and its receptor. Insulin can regulate IGF-I production, acting on the GH receptor or at a post-receptor site. Conversely IGF-I is thought to have a permissive effect on the pancreatic insulin response to glucose.
Growth is compromised in poorly controlled diabetic children; however, a causal link with altered GH/IGF-I levels has not been proven. Insulin-dependent diabetes clearly causes derangements in the GH/IGF-I axis. In poorly controlled diabetics GH levels are invariably raised whilst normal or low levels of IGF-I are found, indicating a dissociation between the two factors. Altered IGF-binding protein levels are also found, with high levels of small binding protein and low levels of large binding protein. These derangements are probably the result of interactions at many levels although the exact mechanisms are not fully understood.
Raised GH levels could result from altered hypothalamic/pituitary control or reduced feedback inhibition. The latter could, in turn, result from low IGF-I levels, reduced availability of IGF-I to relevant receptors or increased levels of inhibitors (possibly the small binding protein). Low IGF-I levels could be directly due to deficient insulin levels or simply to lack of available circulating binding protein.
Alternative or altered molecular forms of circulating GH in diabetes seem unlikely on present evidence.
That GH has an effect on glycaemic control is most evident from the abnormal glucose tolerance seen in acromegalics, but is also seen with physiological GH variations such as during the pubertal growth spurt. In diabetics the derangements to the GH/IGF-I axis, caused by poor metabolic control, leads to aggravation of the metabolic problems.
Altered GH/IGF-I levels have been implicated in the long-term complications associated with diabetes, and whilst GH/IGF-I are not essential for the early changes involved in these complications they may still play an important role in their development, especially proliferative retinopathy.
Activation of the adrenal cortex or the peripheral sympatho-adrenomedullary system does not necessarily influence milk ejection in the rat
Authors: Lau C. 
Published: December 2008

ABSTRACT
Following a 5-h isolation period, primiparous rats have the same milk supply on days 8/9 and 13/14 post partum, yet in response to suckling they release a greater amount of milk at the latter time. Inasmuch as stress is known to inhibit lactation and handling of the pups is stressful to the dams, the question arose as to whether separation from pups before nursing constitutes a greater stress for the dam at the earlier stage of lactation. This possibility was explored in the present study. As an index of stress, changes in plasma corticosterone were measured from chronically cannulated dams. In addition, the role of adrenal hormones and the peripheral sympathetic nervous system in the regulation of milk ejection under these experimental conditions was assessed following bilateral adrenalectomy and treatment with pentolinium, a ganglionic blocker which does not cross the blood–brain barrier. Corticosterone pellets were implanted subcutaneously following adrenalectomy in order to maintain proper lactation. From the results obtained, lactators demonstrated a greater increase in plasma adrenocorticosteroid levels in response to nursing on day 8/9 than on day 13/14 post partum, but milk yield was significantly less at the earlier than at the later stage of lactation. Adrenalectomy in conjunction with corticosterone replacement pellets did not alter milk supply or milk release. The subsequent treatment with pentolinium did not affect milk ejection. Pups still ingested less milk on day 9 than on day 13/14. It is suggested here that the isolation/suckling condition imposed on lactators may be more stressful earlier in lactation. Inasmuch as removal of the adrenal hormones along with ganglionic blockade did not modify the amount of milk ingested by the pups, it is concluded that the smaller milk release observed on day 9 post partum does not result from a direct suppression by the adrenal hormones or by the peripheral sympathetic nervous system on milk ejection.
J. Endocr. (1988) 118, 399–405
Stimulation of release of growth hormone from the anterior pituitary by α-melanocyte-stimulating hormone: a possible mechanism for induction of pseudopregnancy in the rat
Authors: Volosin M. , Celis M. E. 
Published: December 2008

ABSTRACT
In hypophysectomized rats on day 1 of dioestrus, as well as on day 4 of pseudopregnancy, α-MSH (continuous infusion of 1 μg/h) failed to maintain serum concentrations of progesterone. On the other hand, α-MSH did not modify the increase induced by ACTH (1 μg/μl as an infusion plus two additional daily injections of 30 μg/μl), prolactin (200 μg/0·2 ml at 12-h intervals) or GH (300 μg/0·2 ml twice daily) on serum concentrations of progesterone in such rats. However, in intact rats α-MSH caused a significant rise in serum concentrations of GH on day 1 and day 2 of dioestrus. Continuous infusion of α-MSH produced an increase in serum concentrations of GH at 12.00 and 14.00 h on day 1 of dioestrus and at 07.00 h on day 2.
It is therefore suggested that α-MSH may exert its effect by facilitating the secretion of GH, which in turn may induce the release of progesterone.
J. Endocr. (1988) 118, 465–470
Plasma concentrations of insulin-like growth factor-I and insulin in the infant calf: ontogeny and influence of altered nutrition
Authors: Breier B. H. , Gluckman P. D. , Bass J. J. 
Published: December 2008

ABSTRACT
The developmental pattern of plasma insulin-like growth factor-I (IGF-I) and insulin in calves subject to different patterns of weaning was investigated from birth until the age of 6 months. Fifteen male Friesian calves were fed on whole milk (10% of body weight per day) for the first 8 weeks after birth, then allocated into three balanced groups. Group 1 was weaned at 8 weeks; group 2 was weaned at 8 weeks, returned to milk-feeding at 13 weeks to be weaned again at the age of 16 weeks; group 3 was weaned at 12 weeks. After weaning the calves were fed on concentrates and lucerne hay.
At birth, circulating concentrations of IGF-I correlated with birth weight (r = 0·78, P< 0·001). There was a significant (P<0·001) fall in plasma IGF-I from birth (40·3 ± 2·5 μg/l) until 5 weeks (23·8± 1·3 μg/l), and then a gradual (P<0·01) rise until week 8 (35·0 ± 2·2 μg/l). Weaning (groups 1 and 2 after week 8) caused a significant (P<0·01) decrease in plasma IGF-I (20·5 ± 1·9 μg/l); thereafter plasma levels of IGF-I rose gradually (P<0·01) in animals fed on concentrates. The milk-fed calves (group 3) showed a progressive increase in plasma IGF-I with age until they were weaned at 12 weeks (51·0 ± 3·4 μg/l); IGF-I levels then decreased to be similar to group 1 (32·5 ± 2·1 μg/l). When group 2 was returned to milk-feeding, plasma IGF-I concentrations increased to 58·2 ±3·8 μg/l within 4 days and then continued to rise gradually until decreasing upon weaning. The age-related increase in the plasma concentration of IGF-I after 6 weeks was parallel in milk- and concentrate-fed calves.
Binding of 125I-labelled bovine GH to hepatic membranes of neonatal calves was low at birth (specific binding; 1·56 ±0·29% n=3). Somatotrophic binding was apparent at 6 weeks (6·43 ±0·42%, n = 3) and increased (9·2± 1·1%, n=3) at the age of 12 weeks. Thus the early postnatal changes in plasma IGF-I may reflect the transition from GH-independent to GH-dependent IGF-I secretion.
Plasma concentrations of insulin at birth correlated with IGF-I (r = 0·54, P<0·05). However, regression analysis suggested no effect of insulin on birth weight independent of IGF-I. Plasma insulin levels rose gradually until weaning and thereafter were significantly (P<0·01) higher in the milk- than concentratefed calves.
Major changes in plasma concentrations of IGF-I related to monogastric (milk feeding) or ruminant (concentrate feeding) nutrition of the young calf are demonstrated. They may be mediated through changing plasma insulin concentrations. An age-dependent prepubertal rise in plasma IGF-I apparently independent of nutritional factors commenced with the appearance of functional somatotrophic receptors in the liver.
J. Endocr. (1988) 119, 43–50
Growth hormone-deficient dwarfism in the rat: a new mutation
Authors: Charlton H. M. , Clark R. G. , Robinson I. C. A. F. , Goff A. E. Porter , Cox B. S. , Bugnon C. , Bloch B. A. 
Published: December 2008

ABSTRACT
Mutations in animals have provided insight into many aspects of normal and pathological human physiology. This paper reports the discovery and initial characterization of a new mutant dwarf rat. The mutation, inherited as an autosomal recessive, arose spontaneously in a breeding colony of Lewis rats at the Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, Oxford, U.K., in 1985 and the strain has now been established both in Oxford and at Mill Hill. Body growth in the mutant is retarded such that at 3 months of age both males and females weigh approximately 40% less than their normal litter-mates, and continue to grow at a slower rate.
The mutants show a selective reduction in pituitary GH synthesis and storage (pituitary GH concentrations were approximately 10% of normal in males and 6% in females). The concentration of their anterior pituitary trophic hormones (LH, TSH, prolactin and ACTH) were within the normal range in dwarf animals. Exogenous GH treatment for 5 days resulted in an increase in growth rate from 1·5 ± 0·3 to 3·9 ± 0·4 g/day in male mutants, and 0·8 ± 0·2 to 3·1 ±0·1 g/day in females. Longitudinal bone growth rates were more than doubled by this treatment from 49 ± 5 to 100 ±10 μm/day in females and from 52 ± 11 to 131 ± 16 μm/day in males.
Dot blot and Northern blot analysis of pituitary mRNA extracts revealed that the GH message in mutants was between 20 and 25% of normal, and that the GH transcript was of normal size.
Immunoreactive GH-releasing factor (GRF) and somatostatin were present in the dwarf hypothalamus, and exogenous GRF released small amounts of GH in vivo but in proportion to the pituitary GH content. This mutant rat, which shows a selective pituitary GH deficit, may provide a useful new model for studying the endocrinology of growth.
J. Endocr. (1988) 119, 51–58