bluuebunny/crossref_metadata_2025_split huggingface dataset:
The decreased plasma concentration of insulin-like growth factor-I in protein-restricted rats is not due to decreased numbers of growth hormone receptors on isolated hepatocytes
Authors: Thissen J. P. , Triest S. , Maes M. , Underwood L. E. , Ketelslegers J. M. 
Published: December 2008

ABSTRACT
The resistance to GH and the low serum concentrations of insulin-like growth factor-I (IGF-I) that occur during fasting are accompanied by decreased GH receptors in liver homogenates. In protein restriction, however, serum IGF-I but not GH receptors are decreased, suggesting that a post-receptor defect exists. Because conclusions about the status of GH receptors during dietary manipulation are based on studies using liver homogenates, the present study was undertaken to determine whether changes in GH binding by homogenates are paralleled by changes in receptors on the cell surface considered to mediate the GH signal. Collagenase-dispersed hepatocytes or liver homogenates from 7-week-old female Wistar rats fed various diets were evaluated for changes in somatogenic receptors. Fasting for 24 h reduced significantly (P< 0·001) the plasma concentrations of IGF-I (−31%). Likewise, GH-binding sites were decreased on hepatocytes (−55%; P<0·01) and in liver homogenates (−60%; P < 0·001) compared with controls, as was the velocity of initial binding (−77%; P<0·001).
Protein restriction for 1 week decreased plasma concentrations of IGF-I (−42%; P< 0·001) but GH-binding sites were not significantly reduced on hepatocytes or in homogenates. The velocity of initial binding was also not decreased. We conclude that observations on changes in homogenate binding of bovine GH during dietary manipulation provide a reliable means of assessing changes in cell-surface GH receptors. The absence of a decline in surface binding during feeding of a low-protein diet supports the hypothesis that the decline in IGF-I during protein restriction is mediated by post-receptor events.
Journal of Endocrinology (1990) 124, 159–165
Maternal modulation of growth hormone secretion in the neonatal rat: involvement of mother–offspring interactions
Authors: Kacsoh B. , Meyers J. S. , Crowley W. R. , Grosvenor C. E. 
Published: December 2008

ABSTRACT
Serum GH levels increased in 2- or 8-day-old rat pups when sucking mammary glands whose main milk ducts were ligated. Although intragastric administration of rat milk has been shown to increase serum GH levels in neonatal rats, ingestion of milk during suckling did not increase serum GH values further. In another experiment, 2-day-old pups obtained no milk when they were suckled by anaesthetized mothers, and in this instance the serum GH concentration of the pups decreased. This decrease was prevented if the mothers were injected with oxytocin to counteract the depressant effect of the anaesthesia on milk ejection; nevertheless, GH levels in neonatal animals failed to increase following suckling. Thus some aspect of maternal activity appears to be involved in the suckling-induced increase of serum GH in rat pups. To elucidate which components of maternal activity might be involved, the effects of manipulations of ambient temperature as well as stimulation of the oral or anogenital regions were examined. Exposing rat pups to 37 °C (nest temperature) during the 6-h separation period before suckling prevented the separation-induced decrease in serum GH levels of 2-day-old pups. Moreover, exposure to 37 °C for 30 min following a 6-h separation at room temperature (22 °C) mimicked the effect of suckling in increasing serum GH levels in the pups. Suckling following separation at 37 °C was unable to increase serum GH values further. In other studies, stimulation of the oral zone (feeding from a soft cannula) or anogenital zone (inducing urination and defecation with a wet brush) of the pups significantly decreased neonatal serum GH values. The painful stimulus of administration of s.c. hyperosmotic saline was without effect on serum GH levels.
In summary: (1) suckling, even without milk removal, increases serum GH levels in neonatal rats; (2) some aspect of maternal activity is involved in the suckling-induced increase of serum GH concentration in the neonate; (3) provision of a warm ambient temperature by the mother is a critical component of this maternal activity; (4) the effects of milk and the maternal activity associated with suckling are not additive in increasing serum values of GH in neonatal rats; and (5) oral feeding is not a suitable approach for studying the effects of milk on serum GH in neonatal rats.
Journal of Endocrinology (1990) 124, 233–240
Oestrogen positive feedback stimulates the synthesis of LHRH mRNA in neurones of the rostral diencephalon of the rat
Authors: Rosie R. , Thomson E. , Fink G. 
Published: December 2008

ABSTRACT
Our aim was to determine whether oestrogen administered to ovariectomized rats in a manner which stimulates the release of LHRH also stimulates the synthesis of LHRH mRNA. Adult female Wistar rats were ovariectomized under halothane anaesthesia between 09.00 and 11.00 h of dioestrus, immediately injected with either oil or 10 μg oestradiol benzoate (OB) and then killed by cervical dislocation between 16.00 and 17.00 h of the next day (presumptive pro-oestrus). In-situ hybridization carried out with a 30 mer, 32P-labelled, oligonucleotide probe complementary to LHRH mRNA showed that the concentrations of LHRH mRNA in perikarya in the medial preoptic area, diagonal band and medial septum were significantly greater in OB-compared with oil-treated rats. Plasma LH concentrations were significantly increased in three out of four of the OB-treated rats. These results show for the first time that as well as stimulating LHRH and LH release, oestrogen positive feedback also stimulates the synthesis of LHRH mRNA.
Journal of Endocrinology (1990) 124, 285–289
Measurement of parathyroid hormone-related protein in extracts of fetal parathyroid glands and placental membranes
Authors: Abbas S. K. , Pickard D. W. , Illingworth D. , Storer J. , Purdie D. W. , Moniz C. , Dixit M. , Caple I. W. , Ebeling P. R. , Rodda C. P. , Martin T. J. , Care A. D. 
Published: December 2008

ABSTRACT
A radioimmunoassay based on an antiserum to human parathyroid hormone-related protein PTHrP(1–16) was used with PTHrP(1–34) standard to measure the concentration of immunoreactive PTHrP in extracts of fetal parathyroid glands from lambs and calves and also placental membranes obtained from several species, including man. Dilution curves from these sources were parallel to those obtained for PTHrP(1–34) standard. It was demonstrated that this parallelism was not the result of tracer damage caused by enzymic activity in the tissue extracts. Extracts of human placental membranes were subjected to high-pressure liquid chromatography with a linear acetonitrile gradient. Co-elution of cytochemical biological activity with 125I-labelled PTHrP(1–34) was noted. These results provide further evidence for both the fetal parathyroid glands and the placenta containing material resembling PTHrP which may be responsible for sustaining the activity of the placental calcium pump which maintains the fetus hypercalcaemic relative to its mother.
Journal of Endocrinology (1990) 124, 319–325
Effects of bovine 35 kDa FSH-suppressing protein on FSH and LH in rat pituitary cells in vitro: comparison with bovine 31 kDa inhibin
Authors: Robertson D. M. , Farnworth P. G. , Clarke L. , Jacobsen J. , Cahir N. F. , Burger H. G. , de Kretser D. M. 
Published: December 2008

ABSTRACT
The mode of action of a recently isolated gonadal protein, termed FSH-suppressing protein (FSP) or follistatin, on basal and gonadotrophin-releasing hormone (GnRH)-stimulated release of FSH and LH and on pituitary cell content of FSH and LH was examined in rat pituitary cell cultures and compared with the previously reported effects of inhibin. Pituitary cells were cultured for 3–9 days in the presence of graded doses of FSP and the basal release rates and changes in cell contents of FSH and LH determined during this period. FSP suppressed both the basal release rate and the cell content of FSH with median inhibitory concentrations (IC50) of 135 and 161 pmol/l respectively. The corresponding effects of FSP on LH basal release rate and LH cell content (IC50 = 200 pmol/l) were limited compared with the effects on FSH. The effect of FSP on GnRH-stimulated release of FSH and LH during 4 h was determined in cells which had been preincubated with FSP for 3 days, and the GnRH-stimulated release of FSH and LH analysed as a percentage of the respective gonadotrophin available for release. FSP antagonized GnRH action with dose-related increases in the GnRH median effective (stimulatory) concentrations for FSH and LH release (EC50 values = 56 and 400 pmol/l respectively) and a suppression in the maximum release of FSH and LH by excess GnRH (IC50 values =142 and 150 pmol/l respectively). The effect of FSP on FSH cell content after 3 days in culture was insensitive to the neutralizing effects of an inhibin antiserum. The pattern of FSP-induced suppression of FSH basal release and cell content and its inhibition of GnRH-stimulated release of FSH and LH was similar to that observed with inhibin, although FSP is 10–20% as potent as inhibin. When inhibin and FSP were assayed either individually or as a 1:1 (v/v) mixture, the experimentally determined biological activity of the mixture did not differ significantly from that predicted from the individual activities.
It was concluded from the similarity in pituitary responses to FSH and inhibin that FSP is a weak inhibin agonist. Its action can be discriminated from that of inhibin by an inhibin antiserum; however, FSP and inhibin may share a common underlying mechanism of action since their effects are additive.
Journal of Endocrinology (1990) 124, 417–423
Initiation of parturition and lactation in the sow: effects of delaying parturition with medroxyprogesterone acetate
Authors: Whitely J. L. , Hartmann P. E. , Willcox D. L. , Bryant-Greenwood G. D. , Greenwood F. C. 
Published: December 2008

ABSTRACT
The synthetic progestagen, medroxyprogesterone acetate (MPA), was administered to sows in late pregnancy with the objective of slightly delaying the time of farrowing and thereby providing more marked associations between hormonal changes and the termination of pregnancy, and the initiation of farrowing and lactation in this species.
MPA was administered orally (140 mg, twice daily) to eight sows in late pregnancy on days 112, 113 and 114 of gestation. Parturition was then induced to occur on day 116 by injecting 200 μg cloprostenol i.m. on day 115 of gestation. The peripartum changes in the plasma concentrations of progesterone, cortisol, oestradiol-17β, relaxin, prolactin, lactose and 13,14-dihydro-15-keto prostaglandin F2α (PGFM) were measured in these sows together with a group of untreated sows. The gestational length for the MPA-treated sows (116·3 ± 0·3 days, mean±s.e.m.) was significantly (P<0·01) greater compared with the untreated sows (114·9 ± 0·3 days). Plasma progesterone declined earlier (P<0·05) with respect to the time of parturition in the treated sows compared with the untreated group. With respect to the timing of parturition, the time at which maximal concentrations of relaxin were attained and the timing of the subsequent decline were earlier in the MPA-treated sows. In both groups of sows, the concentration of relaxin increased before the decline in plasma progesterone. In the untreated sows, the concentration of PGFM increased either slightly before or at the same time as the decline in plasma progesterone, whereas in sows treated with MPA, progesterone concentrations began to decline before any significant increase in the plasma concentration of PGFM. The profiles of cortisol, oestradiol-17β and PGFM were similar in both groups of sows. In both groups of sows, the timing of the initial increase in the concentration of plasma prolactin coincided with a similar rise in plasma lactose (P<0·01). Plasma progesterone either declined earlier or at the same time as the rise in plasma lactose (P<0·01) in the treated group of sows only.
We conclude that since the prepartum changes in the concentration of progesterone and relaxin occurred before significant changes in the concentration of PGFM in the MPA-treated sows, the nature of the luteolytic factor and the mechanism by which it exerts its action remains obscure. The higher concentration of lactose in the mammary secretion at birth in the MPA-treated sows compared with the untreated group suggested that lactogenesis was initiated earlier with respect to parturition following MPA treatment. Furthermore, the administration of MPA to sows in late pregnancy delayed the onset of parturition but did not inhibit lactogenesis.
Journal of Endocrinology (1990) 124, 475–484
Non-sulphated cholecystokinin in human medullary thyroid carcinomas
Authors: Rehfeld J. F. , Johnsen A. H. , Ødum L. , Bardram L. , Schifter S. , Scopsi L. 
Published: December 2008

ABSTRACT
The expression of gastrin/cholecystokinin (CCK) peptides and their precursors was examined in 16 medullary carcinomas of the human thyroid. Measurements with libraries of sequence-specific radioimmunoassays before and after enzymatic cleavage of extracts and chromatographic fractions showed that the carcinomas contained 1·7 pmol carboxyamidated CCK/g tissue (median; range 0·6–21·8 pmol/g), 0·9 pmol glycine-extended precursor/g (median; range < 0·2–2·3 pmol/g) and 2·3 pmol further COOH-terminal-extended proCCK/g (median; range 0·9–6·2 pmol/g). Neither carboxyamidated gastrins nor any progastrins could be measured. Gel and reverse-phase chromatography revealed only small molecular forms, i.e. > 90% of the amidated immunoreactivity eluted like non-sulphated CCK-8 or CCK-7. The results show that human medullary thyroid carcinomas synthesize CCK peptides. The predominance of non-sulphated CCK is unusual. Taken together with earlier observations from dogs and pigs, our results raise the possibility that small non-sulphated CCK peptides modulate thyroid C-cell secretion in an autocrine manner.
Journal of Endocrinology (1990) 124, 501–506
AMYLIN AND AMYLIN-AMIDE LACK AN ACUTE EFFECT ON BLOOD GLUCOSE AND INSULIN
Authors: Ghatei M. A. , Datta H. K. , Zaidi M. , Bretherton-Watt D. , Wimalawansa S. J. , MacIntyre I. , Bloom S. R. 
Published: December 2008

ABSTRACT
Amylin-amide has been implicated in the pathogenesis of type II diabetes due to its proposed inhibitory effect on insulin release from β cells of the pancreatic islets, and on glucose uptake by the skeletal muscle. In experiments with rats and rabbits we failed to demonstrate these anti-insulin actions of amylin and amylin-amide. A single bolus dose of the two peptides (500 pmol) administered i.v. failed to supress plasma insulin levels or to elevate blood glucose levels. The continuous infusion of amylin-amide into rabbits also failed to supress the release of insulin in response to hyperglycaemia produced by an i.v. bolus injection of glucose. These in vivo observations imply that the amylin peptides may not have a primary physiological role in carbohydrate metabolism, but in view of our previous findings, we speculate that the peptide has a more prominent role in calcium homeostasis.
Effect of low temperatures on glucose-induced insulin secretion and glucose metabolism in isolated pancreatic islets of the rat
Authors: Escolar J. C. , Hoo-Paris R. , Castex Ch. , Sutter B. Ch. J. 
Published: December 2008

ABSTRACT
The direct effect of hypothermia on the inhibition of insulin secretion may result from inhibition of the availability of energetic substrates and/or the lack of metabolic signals. In order to verify this hypothesis, the insulin secretion and the main metabolic glucose pathways were measured during the incubation of rat islets. In the presence of 16·7 mmol glucose/l and at 37 °C, insulin secretion was 925 ± 119 μU/2 h per ten islets. With the same experimental conditions, glucose utilization, determined as the formation of 3H2O from [5-3H]glucose was 2225 ±184 pmol/2 h per ten islets, glucose oxidation measured as the formation of 14CO2 from [U-14C]glucose was 673 ± 51 pmol/2 h per ten islets, pentose cycle determined as the formation of 14CO2 from either [1-14C]glucose or [6-14C]glucose was 37 ± 5 pmol/2 h per ten islets; glucose oxidation by the tricarboxilic acid cycle, calculated to be the difference between glucose oxidation and pentose cycle values, was 636 pmol/2 h per ten islets.
Hypothermia highly inhibited glucose-induced insulin secretion and glucose utilization. Inhibition of insulin secretion was partial at 27 °C since it was 2·5 times lower than that at 37 °C, and it was complete at 17 °C. Glucose oxidation in the tricarboxilic acid cycle was markedly inhibited by hypothermia since the inhibition coefficient (Q10) between 37 and 27 °C was 5. In contrast, glucose oxidation in the pentose phosphate shunt was enhanced at 27 °C, reaching 92 ± 17 pmol/2 h per ten islets, and it was inhibited relatively little at 17 °C.
These results suggest that hypothermia markedly inhibits glucose metabolism with the exception of the pentose pathway which could play an important role by inducing the insulin secretion at 27 °C.
Journal of Endocrinology (1990) 125, 45–51
Vasopressin responses to hypoxia in conscious rats: interaction with water restriction
Authors: Griffen S. C. , Raff H. 
Published: December 2008

ABSTRACT
The purpose of this study was to determine the effect of water restriction on the vasopressin response to hypoxia in conscious Long–Evans rats. Rats were prepared with chronic indwelling femoral artery and vein catheters 1 week before experimentation. At 24 h before the first blood sample, the supply of drinking water was maintained ad libitum (water replete) or removed (water deplete). At 24 h, a control blood sample was taken and then normoxia (21% O2) was maintained or hypoxia (10% O2) induced. Additional blood samples were taken at 1, 18 and 24 h. All blood samples (2·5 ml) were simultaneously replaced with donor blood to maintain isovolaemia. Hypoxia led to a very small and transient increase in vasopressin in the water-replete rats. The combination of hypoxia and water restriction led to a greatly augmented vasopressin response at 1 h (60 ± 16 pmol/l); this response was also not sustained. Additional non-cannulated rats were exposed to 24 h of normoxia or hypoxia with or without water available ad libitum and posterior pituitaries were collected after decapitation for measurement of vasopressin content. Water restriction, hypoxia and water restriction plus hypoxia all led to decreased pituitary vasopressin content. We conclude that the vasopressin response to hypoxia in conscious rats is small and transient, and that concomitant water restriction augments the vasopressin response to acute but not chronic hypoxia.
Journal of Endocrinology (1990) 125, 61–66
Hypoinsulinaemia in the lactating rat is caused by a decreased glycaemic stimulus to the pancreas
Authors: Madon R. J. , Ensor D. M. , Flint D. J. 
Published: December 2008

ABSTRACT
An in-vitro perifusion system was devised in order to examine the secretory profiles of isolated islets of Langerhans, derived from different physiological states, when subjected to various stimuli relevant to lactation. Islets from pregnant rats secreted more insulin than did those from virgin animals; however, islets from lactating and virgin animals secreted similar amounts of insulin with all stimuli, including glucose, amino acids, cations and neurotransmitters. When virgin rats were pretreated for 5 days in vivo with GH or prolactin, insulin responses in vitro were unchanged. Cannulation of the hepatic portal vein and inferior vena cava in vivo revealed that both insulin and glucose concentrations were lower in the portal vein of the lactating rat compared with the virgin animal. It was therefore concluded that insulin concentrations are depressed during lactation as a consequence of the pancreas receiving a diminished glycaemic stimulus rather than because of any change in β-cell sensitivity.
Journal of Endocrinology (1990) 125, 81–88
Modulation of growth hormone (GH) secretion and GH mRNA levels by GH-releasing factor, somatostatin and secretagogues in cultured bovine adenohypophysial cells
Authors: Tanner J. W. , Davis S. K. , McArthur N. H. , French J. T. , Welsh T. H. 
Published: December 2008

ABSTRACT
The effects of endogenous hypothalamic neurohormones and activators of second messenger signalling systems on the secretion of GH and on cell content of GH mRNA of cultured bovine adenohypophysial cells were studied. Synthetic bovine GH-releasing factor (bGRF; 100 nmol/l) increased secretion of GH by bovine adenohypophysial cells five-fold relative to control. Forskolin (an adenyl cyclase activator; 10 μmol/l) and the synthetic cyclic AMP analogue dibutyryl cyclic AMP (dbcAMP; 1 mmol/l) increased secretion of GH by 1·9- and 1·7-fold respectively, relative to control. The protein kinase C activator phorbol 12-myristate 13-acetate (PMA), provided at 1 μmol/l or 10 nmol/l, increased GH secretion by 6·6- and four-fold respectively, relative to control. Somatostatin-14 (SRIF-14) attenuated basal, bGRF-, forskolin- and dbcAMP-stimulated secretion of GH by 40, 49, 47 and 67% respectively, but did not, however, diminish PMA-stimulated GH secretion. The content of GH mRNA in cultured bovine adenohypophysial cells increased 2·2-, 1·7- and 3·2-fold by administration of bGRF, forskolin and PMA respectively, relative to control. Although GH mRNA content was unchanged by SRIF-14 treatment relative to control, SRIF-14 did reduce bGRF-stimulated bGH mRNA content by 67%. This study demonstrates that mechanisms subserving GH secretion in bovine adenohypophysial cells (e.g. adenyl cyclase and protein kinase C) may be coupled with mechanisms which regulate expression of the GH gene or with factors affecting message stability.
Journal of Endocrinology (1990) 125, 109–115
Serum concentrations of thyroid hormones and activity of iodothyronine deiodinase in peripheral tissues of the house musk shrew, Suncus murinus
Authors: Tsukahara F. , Muraki T. , Nomoto T. 
Published: December 2008

ABSTRACT
Serum concentrations of thyroid hormones and the properties of iodothyronine deiodinase in tissues of the house musk shrew, Suncus murinus, were examined and compared with those of the rat. Serum concentrations of thyroxine (T4) and 3,3′,5′-tri-iodothyronine (rT3) were higher, while the serum concentration of 3,5,3′-tri-iodothyronine (T3) was lower in the shrew than in the rat. Among liver, kidney, skeletal muscle, heart, brown adipose tissue (BAT), spleen, lung, testes and thymus homogenates of the shrew, T4 5′-deiodinase (5′D) activity was highest in BAT, and rT3 5′D activity was highest in both the liver and BAT. Intermediate or low T3 5-deiodinase activity was noted in all tissues examined. Activity of 5′D for T4 and rT3 in liver and kidney was much lower, while that of BAT was much higher in the shrew than in the rat. Liver and kidney 5′D may be type-I and that of BAT may be type-II in the shrew, judging from its response to 6-n-propyl-2-thiouracil and iopanoic acid and substrate preference. Thus 5′D of the shrew was similar to that of the rat in type, but was different with respect to its activity in some peripheral tissues. This difference may have relevance to the low T3 state of the shrew.
Journal of Endocrinology (1990) 125, 117–122