bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intermittent protein–calorie malnutrition in the young rat causes long-term impairment of the insulin secretory response to glucose in vitro
Authors: Swenne I. , Crace C. J. , Jansson L. 
Published: December 2008

ABSTRACT
The effect of a limited period of protein–calorie malnutrition in young rats on insulin secretion in the adult has been studied. Three-week-old rats were weaned onto diets containing 5% protein (low protein; LP) or 15% protein (control; C) and maintained for 3 weeks on their respective diets. A third experimental group was weaned onto standard rat chow (18% protein; normal diet; N). From 6 weeks of age onwards all rats were fed the standard rat chow. Pancreatic islets were isolated from rats aged 3, 6 and 12 weeks and their insulin secretory response to glucose or arginine was tested. At 12 weeks the effects of the secretagogues were also tested using perfusion of isolated pancreatic glands.
In islets from 6-week-old LP rats the glucose-stimulated insulin release was only 25% of that of C and N rats of the same age. Islets from C and N rats responded to arginine in the presence of a low glucose concentration with a small increase in insulin secretion, whereas no such response could be demonstrated in islets from 6-week-old LP rats. Islets from 6- and 12-week-old N rats responded to glucose and arginine. Islets from 12-week-old C rats had a similar response to glucose but did not respond to arginine in the presence of a low glucose concentration. In islets from 12-week-old LP rats the secretory response to glucose remained only 40% that of C and N rats and there was no response to arginine in the presence of a low glucose concentration. The observations on the secretory response of isolated islets from 12-week-old rats were paralleled by similar findings with the perfused, isolated pancreas.
It is concluded that protein–calorie malnutrition early in life persistently impairs the insulin secretory response of the B cell. The individual may, as a consequence, have a lowered ability to respond to nutritional and diabetogenic challenges and it is thus possible that early protein–calorie malnutrition predisposes for diabetes.
J. Endocr. (1988) 118, 295–302
Major secretory protein of human decidualized endometrium in pregnancy is an insulin-like growth factor-binding protein
Authors: Bell S. C. , Patel S. R. , Jackson J. A. , Waites G. T. 
Published: December 2008

ABSTRACT
Pregnancy-associated endometrial α1-globulin (α1-PEG) is quantitatively the major secretory protein product, synthesized and secreted in vitro, of the human decidualized endometrium during pregnancy. This protein has been purified from cytosolic extracts of this tissue and has now been characterized as a 32 kDa somatomedin/insulin-like growth factor (IGF)-binding protein. Immunoreactive α1-PEG isolated from amniotic fluid exhibited identical physiochemical properties and IGF-I-binding characteristics. In cytosolic extracts of pregnancy endometrium, in incubation medium of this tissue and in amniotic fluid, the 32 kDa protein represented the major α1-PEG immunoreactive protein and major IGF-I-binding component. Purified α1-PEG and incubation medium of pregnancy endometrium competed for IGF-I with placental membrane IGF receptors in vitro. The implications of the endometrial source of IGF-I-binding protein are dicussed with reference to the origin of the amniotic fluid and serum small Mr IGF-binding protein and to the suggested paracrine effect upon trophoblast proliferation.
J. Endocr. (1988) 118, 317–328
Day–night rhythm of 5-methoxytryptamine biosynthesis in the pineal gland of the golden hamster (Mesocricetus auratus)
Authors: Galzin A. M. , Eon M. T. , Esnaud H. , Lee C. R. , Pévet P. , Langer S. Z. 
Published: December 2008

ABSTRACT
5-Methoxytryptamine is a potent agonist of presynaptic 5-hydroxytryptamine autoreceptors modulating serotonin release in the central nervous system. This methoxyindole can be synthesized in the pineal gland, but its presence in vivo is still controversial, probably because of rapid catabolism by monoamine oxidase. An improved high-pressure liquid chromatography method, with coulometric detection, has been developed for the simultaneous measurement of melatonin, 5-methoxytryptamine, 5-methoxytryptophol and 5-methoxyindolacetic acid. We have demonstrated a day–night rhythmicity in the amount of 5-methoxytryptamine in the pineal gland of golden hamsters (Mesocricetus auratus) maintained under a long photoperiod (14 h light: 10 h darkness) and pretreated with the monoamine oxidase inhibitor pargyline. Levels of 5-methoxytryptamine were highest at 16.30 h and lowest at 00.30 h. The rhythm for 5-methoxytryptamine appears to be the same as for serotonin (opposite in phase to that of melatonin). The identification of 5-methoxytryptamine has been confirmed by analysis with gas chromatography–mass spectrometry.
J. Endocr. (1988) 118, 389–397
AUTOCRINE REGULATION OF CASEIN TURNOVER IN GOAT MAMMARY EXPLANTS
Authors: Stewart G. M. , Addey C. V. P. , Knight C. H. , Wilde C. J. 
Published: December 2008

ABSTRACT
Local feedback control of milk protein secretion was investigated in goat mammary explants by measuring degradation of newly synthesized casein in the presence of a goat milk whey fraction. Reduced net synthesis of [3H]casein in the presence of the milk fraction was due, at least in part, to its degradation during secretion, suggesting that this process is under autocrine regulation.
INFLUENCE OF GERM CELLS UPON TRANSFERRIN SECRETION BY RAT SERTOLI CELLS in vitro
Authors: LE MAGUERESSE B. , PINEAU C. , GUILLOU F. , JEGOU B. 
Published: December 2008

ABSTRACT
Indirect approach (hypotonic treatment) and direct approaches (co-cultures and conditioned media) were used in order to investigate the effects of germ cells from adult rats upon transferrin secretion by Sertoli cell cultures prepared from 20-day-old rats. Removal of germ cells contaminating the Sertoli cell cultures resulted in a significant decrease in transferrin secretion whereas the addition of crude germ cell preparations or of enriched preparations of pachytene spermatocytes, early spermatids and of liver epithelial cells (LEC) markedly stimulated this parameter. Furthermore, spent media of pachytene spermatocytes and of early spermatids, but not of LEC, also stimulated transferrin production. It is concluded that germ cells normally located within the adluminal compartment of the seminiferous tubules may be capable of controlling their own supply of iron via their influence upon transferrin secretion by the Sertoli cells.
Neuropharmacological analysis of the control of LH secretion in gonadectomized male and female rats: altered hypothalamic responses to inhibitory neurotransmitters in long-term castrated rats
Authors: Almeida O. F. X. , Nikolarakis K. E. , Herz A. 
Published: December 2008

ABSTRACT
The control of LHRH and LH by neurotransmitters and neuromodulators such as the endogenous opioid peptides is essentially the same in intact adult male and female rats: adrenergic and dopaminergic agonists stimulate LH release and opioid agonists inhibit it. Several weeks after gonadectomy, however, the contribution of the endogenous ligands of adrenergic, dopaminergic and opioidergic receptors to the control of LHRH is altered. A detailed pharmacological analysis in long-term ovariectomized females confirmed previous reports that adrenergic and dopaminergic agonists still enhance secretion of LHRH and LH and opioid receptor agonists still suppress it. A similar investigation in long-term castrated males also confirmed previous reports that opioid agonists fail to block LH secretion. In addition, we have found that while adrenergic and dopaminergic agonists cause increases in serum concentrations of LH, adrenoreceptor and dopamine receptor antagonists do not inhibit LH release in long-term castrates. Furthermore, the opioid antagonist naloxone does not raise serum LH levels in either sex after long-term gonadectomy. These observations therefore imply reduced opioidergic, dopaminergic and adrenergic transmission, in relation to LHRH release, after longterm castration. In addition, opioid receptor activity (assessed by responsiveness to an opioid receptor agonist) of female rats is maintained, whereas that of male rats is lost, after long-term gonadectomy.
J. Endocr. (1988) 119, 15–21
The anabolic actions of growth hormone and thyroxine on protein metabolism in Snell dwarf and normal mice
Authors: Bates P. C. , Holder A. T. 
Published: December 2008

ABSTRACT
The individual effects of GH and thyroxine (T4) on protein metabolism were determined in dwarf and normal mice in vivo. The hormone deficiencies of dwarf mice (low serum concentrations of GH and T4) resulted in decreased protein synthesis rates in skeletal muscle and liver, but no difference in synthesis rates in heart. The efficiency of synthesis (g protein/g RNA per day; KRNA) was lower in all three tissues in dwarf compared with normal mice, but effects on RNA concentration were not consistent; there was no change in muscle, a decrease in liver and an increase in heart.
Treatment of dwarf mice for 9 days with either human GH or T4 caused increases in body weight and length. Protein synthesis rates were increased in muscle, liver and heart by either hormone, though much more so with T4 than GH. In muscle and liver both GH and T4 treatment resulted in an increased RNA concentration, but T4 treatment also increased KRNA. In heart, both GH and T4 increased KRNA with no change in RNA concentration. GH caused no significant changes in protein degradation rates so that growth rates were increased. T4 increased degradation rates so that there was no increased net growth in muscle or liver; in heart, T4 did induce increased growth despite the large increase in degradation rate. Tibial length was increased by both hormones; GH treatment of dwarf mice also increased cartilage sulphate incorporation on day 9, but T4 treatment did not, suggesting that bone growth is transient with T4 treatment.
Normal mice showed no changes in growth or tissue protein metabolism in response to GH, but following T4 treatment there was increased protein turnover due to higher tissue RNA concentrations, although only heart growth was increased. Thus normal mice showed almost no net response to GH or T4, but dwarf mice showed a large response to both hormones. The response was different, however, in that GH caused concomitant increases in growth rates whereas T4 altered body tissue proportions.
J. Endocr. (1988) 119, 31–41
Corticotrophin-releasing factor immunoreactivity in the hypothalamus of the rat during the perinatal period
Authors: Chatelain A. , Boudouresque F. , Chautard T. , Dupouyt J. P. , Oliver C. 
Published: December 2008

ABSTRACT
Corticotrophin-releasing factor-41 (CRF-41) immunoreactivity has been measured in hypothalamic extracts of fetal (on days 17, 19 and 21 of gestation), neonatal (1, 2, 3 and 4 weeks of age) and adult rats with a specific radioimmunoassay developed for synthetic rat CRF-41. The hypothalamic content (fmol) and concentration (fmol/mg protein) of immunoreactive CRF-41 gradually increased with age. Chromatography of hypothalamic extracts on Sephadex G-50 Fine showed one single peak of immunoreactive CRF-41 which co-eluted with synthetic rat CRF-41. The retention time of hypothalamic CRF-41 during high-performance liquid chromatography was identical to that of synthetic rat CRF-41 at all stages investigated. These results are consistent with the development of neurones containing CRF-41-like molecules in both the hypothalamus and the median eminence of the fetus, as well as with the hypothalamic control of the cortico-stimulating function of the pituitary gland as early as day 19 of gestation.
J. Endocr. (1988) 119, 59–64
Effects of dietary sodium restriction on peptide stimulation of aldosterone secretion by the isolated perfused rat adrenal gland in situ: a report of exceptional sensitivity to angiotensin II amide
Authors: Hinson J. P. , Vinson G. P. , Whitehouse B. J. 
Published: December 2008

ABSTRACT
The effects of prior sodium depletion on the steroidogenic responses of the rat adrenal gland have been investigated using a method of perfusing the isolated adrenal gland of the rat in situ. Secretion rates of aldosterone in response to the known adrenocortical stimulants ACTH, angiotensin II amide and α-MSH were measured. In each case, the adrenals from sodium-deplete animals responded to a lower dose of the stimulant than the normal animals. This resulted in a 10-fold increase in sensitivity to ACTH, a 100-fold increase in sensitivity to angiotensin II amide, and a 1000-fold increased sensitivity to α-MSH, bringing the threshold concentration required for aldosterone secretion into the physiological range of α-MSH concentrations.
The perfused adrenal gland is particularly sensitive to angiotensin II amide; a bolus administration of 1 amol gave a significant increase in aldosterone secretion in the sodium-deplete group.
These data confirm previous reports of increased adrenal sensitivity to α-MSH and angiotensin II in sodium depletion, and also suggest the existence of intraglandular mechanisms for signal amplification which may be involved in mediating the adrenal response to very small concentrations of stimulant.
J. Endocr. (1988) 119, 83–88
Lack of an effect of morphine or naloxone on the oestrogen-induced LH surge in anoestrous ewes
Authors: Horton R. J. E. , Clarke I. J. 
Published: December 2008

ABSTRACT
To determine whether opioid mechanisms modulate the positive feedback effect of oestrogen on LH secretion, anoestrous ewes were given a single injection of 50 μg oestradiol benzoate (OB), followed by infusions of morphine or naloxone. All sheep were injected i.m. with 50 μg OB at 00.00 h. In experiment 1, sheep were given i.v. infusions of the following: group 1, 12 ml saline/h from 09.00 to 15.00 h (n=12); group 2, 40 mg naloxone/h from 09.00 to 12.00 h (n = 5); group 3, 40 mg naloxone/h from 10.00 to 14.00 h (n = 5); group 4, 10 mg morphine/h from 09.00 to 15.00 h (n = 5); and group 5, 20 mg morphine/h from 09.00 to 15.00 h (n = 5). Jugular blood samples were taken at 30-min intervals to monitor LH surges, which commenced 13.0 ± 0·6 h after injection of OB in control (OB plus saline) ewes. The infusions of naloxone or morphine did not affect the timing or magnitude of the oestrogen-induced LH surge.
To examine the possibility that opioidergic regulation of the LH surge occurred earlier than the infusion regimens in experiment 1, sheep were infused from the time of the OB injection (00.00 h) until 15.00 h. In this experiment (experiment 2), sheep were given i.v. infusions of the following: group 1, 4·2 ml saline/h (n=5); group 2, 20 mg naloxone/h (n=5); and group 3, 20 mg morphine/h (n=5). As in experiment 1, treatment with neither the opioid agonist or antagonist was able to alter the positive feedback response of OB.
These results suggest that neither the timing of the LH surge or the peak concentrations of LH achieved in plasma are influenced by opiates in this model. This suggests that in contrast to the rat, the mechanisms responsible for generating the oestrogen-induced preovulatory-like LH surge in the anoestrous ewe do not involve any endogenous opioid peptide mechanisms.
J. Endocr. (1988) 119, 89–93
Effect of growth hormone on growth and myelination in the neonatal hypothyroid rat
Authors: King R. A. , Smith R. M. , Meller D. J. , Dahlenburg G. W. , Lineham J. D. 
Published: December 2008

ABSTRACT
The possible involvement of a deficit of GH and insulin-like growth factor-I (somatomedin C) (IGF-I/SMC) in mediating the effects of propylthiouracil (PTU)-induced hypothyroidism on body and skeletal growth and myelination was studied in the neonatal rat. Myelination (as assessed by 2′,3′-cyclic nucleotide 3′-phosphohydrolase (CNP) activity), skeletal growth (as assessed by tail length) and body weight of pups from PTU-treated mothers were significantly retarded compared with normal animals or euthyroid controls. At 20 days after birth, plasma GH in hypothyroid animals was undetectable (< 10 μg/l), pituitary GH content was 1 ·2% of control, and plasma, liver and kidney IGF-I/SMC concentrations were 63, 68 and 50% of control values respectively. CNP activity in hypothyroid brain was 52% of normal controls but the concentration of IGF-I/SMC was 113–154% of control. Treatment of hypothyroid animals from day 1 with GH (10 mg/kg body weight per day) restored liver and plasma IGF-I/SMC concentrations at 20 days to values above those of normal animals and euthyroid controls. The concentration of IGF-I/SMC was also significantly (P< 0·001) restored in hypothyroid kidney (79% of normal), but the concentration in brain was unaffected. These observations provide evidence that the GH treatment employed in the present experiments was adequate to restore the deficit. GH treatment had no significant effect on tail length or CNP activity, and only a small (4–24%) effect on body weight at 20 days. Only thyroxine was able fully to restore body weight and substantially restore tail length and CNP activity.
The present study provides strong evidence against an important involvement of GH or IGF-I/SMC in mediating the effects of thyroid hormone on myelination and body growth in the infant rat. It does not, however, rule out the possibility that thyroid hormone is required for the expression of the growth-promoting effects of IGF-I/SMC by other mechanisms such as the expression of the IGF-I/SMC receptor.
J. Endocr. (1988) 119, 117–125
The presence of atrial natriuretic peptide in canine cerebrospinal fluid and its possible origin in the brain
Authors: Marumo F. , Masuda T. , Masaki Y. , Ando K. 
Published: December 2008

ABSTRACT
The presence of atrial natriuretic peptide (ANP) in canine cerebrospinal fluid (CSF) was clearly demonstrated and an attempt was made to determine its origin as either the brain or the atrium. The concentration of ANP in canine CSF was 0·78 ±0·37 pmol/l (n = 31) and showed no evident correlation with that in plasma (r =0·12). Physiological doses of human α-ANP (α-hANP) were continuously infused intravenously into nine dogs, and ANP concentrations in CSF and plasma were examined six to eight times within a 120-min period following this. The ANP level in CSF was not influenced by the systemic administration of α-hANP up to 180 min. Only one low molecular weight peak corresponding to α-hANP could be obtained from the CSF samples, while both low and high molecular weight peaks were observed for plasma ANP by gel permeation chromatography. In the atrial and hypothalamic tissue extracts the same kinds of peaks were also evident.
These results prove the presence of ANP in canine CSF and that it does not come from blood that has seeped across the blood–CSF barriers, but suggest that it may originate from the brain.
J. Endocr. (1988) 119, 127–131
β-Adrenergic blockade counteracts starvational ketosis, but aggravates post-exercise ketosis in non-athletes
Authors: Vahed Y. A. K. , Koeslag J. H. , de V. Lochner J. 
Published: December 2008

ABSTRACT
Post-exercise ketosis is not abolished by glucose ingestion immediately after exercise but is counteracted by simultaneous β-adrenergic blockade. To investigate the effect of β-adrenergic blockade on post-exercise ketosis without the ingestion of glucose, we administered propranolol (1 mg/kg body mass) to 15 carbohydrate-starved people, of whom five had just walked 9 km in 2 h. There were 43 control subjects (no propranolol). The blood concentration of 3-hydroxybutyrate rose from 0·18 ± 0·02 (s.e.m.) mmol/l at 07.00 h to 0·35 ±0 04 mmol/l at 09.00 h whether the subjects had exercised during those 2 h or not (d.f. = 57). The blood concentration of 3-hydroxybutyrate at 15.00 h in the groups not treated with propranolol was not affected by exercise (0·95 ± 0·90 mmol/l; d.f. = 42). Propranolol significantly raised the concentration of 3-hydroxybutyrate at 15.00 h to 1·68 ±0·26 mmol/l when given after exercise (d.f. = 4), but lowered it to 0·46 ±0·07 mmol/l in the non-exercised group (d.f. = 9). This was not accompanied by significant differences in the blood concentrations of glucose, free fatty acid, insulin or glucagon. The difference in response to propranolol administration is probably determined by the alanine and lactate flux from muscle for hepatic oxaloacetate synthesis.
J. Endocr. (1988) 119, 167–171
Influence of blood calcium on calcitonin receptors in isolated chick osteoclasts
Authors: Eliam M. C. , Baslé M. , Bouizar Z. , Bielakoff J. , Moukhtar M. , de Vernejoul M. C. 
Published: December 2008

ABSTRACT
Isolated osteoclasts obtained from young chickens fed a normal (+ Ca) or deficient ( − Ca) calcium and vitamin D diet for 3 weeks, were studied for their ability to bind salmon calcitonin (sCT). Osteoclasts obtained from −Ca chickens, when incubated with 0·1 μmol sCT/l, doubled cyclic (c)AMP production and retracted from a glass support, as observed by scanning electron microscopy. The presence of receptors was also demonstrated by autoradiography and competition analysis of 125I-labelled sCT binding. The number of receptors per cell was 0·9 ± 0·1 × 104. In contrast, osteoclasts obtained from + Ca chickens did not increase cAMP production and did not retract in the presence of 0·1 μmol sCT/l. No specific binding of 125I-labelled sCT could be demonstrated on these osteoclasts.
Plasma levels of calcium and calcitonin were measured in +Ca and − Ca chickens. The plasma concentration of calcium was markedly lower at 3 weeks in −Ca than in +Ca chickens. The plasma concentration of calcitonin was decreased in − Ca chickens compared with +Ca chickens at the first week and kept decreasing during the 3 weeks.
These results strongly support the hypothesis that calcium and vitamin D intake regulate plasma calcitonin levels in chickens, and that calcitonin receptors can be detected on chicken osteoclasts only when blood calcium is decreased by a diet deficient in calcium and vitamin D.
J. Endocr. (1988) 119, 243–248