bluuebunny/crossref_metadata_2025_split huggingface dataset:
ACTH and adrenal aerobic glycolysis. II: Effects of aminoterminal peptide fragments on lactic acid and steroid production by mouse adrenocortical cells
Authors: Hinson J. , Birmingham M. K. 
Published: December 2008

ABSTRACT
The effects of shortening the ACTH molecule from either end of the peptide chain on adrenal glycolysis and steroidogenesis were examined in mouse adrenal cell suspensions. Shortening the (1–24) sequence to (1–17), (1–16) and (1–14), thereby interfering with the basic tetrapeptide (15–18) assigned to the address message, progressively reduced both glycolytic and steroidogenic potencies by four, six and ten orders of magnitude respectively, without impairing the capacity for maximal excitation. The glycolytic potency of the (1–18) sequence, which was amidated at the C-terminal, equalled that of ACTH(1–24), but the steroidogenic potency was reduced by an order of magnitude. The (1–13) sequence of α-MSH, which contains substitutions at both terminals, had glycolytic and steroidogenic potencies intermediate between those of ACTH(1–16) and ACTH(1–17). Deletion of Ser1,Tyr2 from ACTH(1–18)-NH2 reduced both potencies by an order of magnitude. ACTH(11–24) and (7–38) were inactive or inhibitory.
The capacity for excitation was further examined by comparing responses to peptide fragments (1–4), (1–10), (1–13), (4–10), (4–11), (5–10), (5–14), (7–13) and (11–24) at a concentration of 1 mmol/l. All fragments, excepting (1–4), (5–10) and (11–24) were active. The activities of fragments (5–14) and (7–13), as opposed to (5–10), suggest that the requirements for methionine in position 4 may be replaced by the (11–13) tripeptide. The relative glycolytic responses of fragments containing the (11–13) sequence exceeded the steroidogenic responses, suggesting that the (11– 13) sequence may be specifically implicated in a receptor involved in glycolysis. With this exception, the functional domains within the ACTH molecule responsible for excitation, potentiation and affinity appear to be in similar locations for both evocation of glycolysis and steroidogenesis, judging from the parallel responses to reduction in chain length.
J. Endocr. (1987) 115, 71–76
Sexual activity increases plasma concentrations of cholecystokinin octapeptide and offsets hunger in male rats
Authors: Linden A. , Hansen S. , Bednar I. , Forsberg G. , Södersten P. , Uvnäs-Moberg K. 
Published: December 2008

ABSTRACT
Male rats deprived of food for 48 h ignored food pellets immediately after ejaculating with a sexually receptive female rat as did males tested 5 min after i.p. injection of 5 μg cholecystokinin octapeptide (CCK-8) or males which had consumed food pellets for 1 h. The concentration of CCK-8 in plasma was increased to comparable levels (10·1±3·8 (s.e.m.); 11·3 ± 3·7 and 7·2± 0·5 pmol/l respectively, compared with 1·2 ± 0·3 pmol/l for NaCl-injected controls) under each of these conditions, whereas the concentration of gastrin increased only after food consumption (18·4 ± 3·8; 17·7 ± 5·4 and 54·3± 7·0 pmol/l respectively, compared with 21·5 ± 2·1 pmol/l for NaCl-injected controls). The effect of ejaculation on the latency to starting to eat was partially reversed by i.p. injection of 50 mg of the CCK-8 antagonist proglumide, but neither treatment with proglumide or CCK-8 nor consumption of food affected the display of sexual behaviour. The results support the suggestion that CCK-8 is a 'satiety peptide' in the rat.
J. Endocr. (1987) 115, 91–95
Effect of 1,25-dihydroxyvitamin D3 on plasma concentrations of calcium-binding protein in normal and rachitic (vitamin D-dependent rickets type I) pigs
Authors: Maunder E. M. W. , Pillay A. V. , Care A. D. 
Published: December 2008

ABSTRACT
An i.v. injection of calcitriol (1,25-(OH)2D3) had no effect within 2·5 h on plasma concentrations of calbindin-D9k (vitamin D-induced calcium-binding protein; CaBP) in hypocalcaemic pigs with inherited vitamin D-dependent rickets type I or in their normocalcaemic siblings or half-siblings. Three days later the plasma concentration of CaBP had doubled in the hypocalcaemic pigs, but was unaltered in the normocalcaemic siblings and half-siblings. Following daily i.v. injections of 1,25-(OH)2D3 for a further 5 days (days 4–8) plasma concentrations of CaBP increased in both the hypocalcaemic (days 4–8) and normocalcaemic (day 8) pigs, the effect being more rapid and greater in the hypocalcaemic 1,25-(OH)2D3-deficient animals. An i.v. injection of 1,25-(OH)2D3 to pure Yucatan pigs also had no effect on plasma concentrations of CaBP within 1·5 h, but in the following 1 h there was some indication of an increase in plasma CaBP levels.
In contrast to the normal pigs, insulin-induced hypoglycaemia did not lead to a peak in plasma CaBP concentrations in the hypocalcaemic pigs. There was also no change in the plasma concentrations of 1,25-(OH)2D3 associated with the peak in plasma CaBP following insulin-induced hypoglycaemia in normocalcaemic pigs. These results suggest that changes in plasma concentrations of 1,25-(OH)2D3 are not directly involved in mediating the increase in plasma CaBP which follows hypoglycaemia induced by insulin in normal pigs, although 1,25-(OH)2D3 probably plays a permissive role.
J. Endocr. (1987) 115, 129–134
Growth hormone induction of insulin-like growth factor I messenger RNA in primary cultures of rat liver cells
Authors: Norstedt G. , Möller C. 
Published: December 2008

ABSTRACT
Primary liver cells from adult rats were used to study the hormonal regulation of mRNA coding for insulin-like growth factor I (IGF-I). IGF-I mRNA could be detected at a low concentration in liver cells prepared from hypophysectomized rats and cultivated for 3 days. When these cells were exposed to GH on the second day, a dose-dependent increase in IGF-I mRNA was observed. The continuous presence of serum was not a prerequisite for this response, since GH also induced IGF-I mRNA in a defined hormone-supplemented medium. It is concluded that GH can induce IGF-I mRNA in the liver by a direct mechanism.
J. Endocr. (1987) 115, 135–139
Modulation by continuous oestrogen treatment and by progesterone of oestrogen receptors in the rabbit uterus
Authors: Batra S. , Owman Ch. , Rydhström H. , Sjöberg N.-O. 
Published: December 2008

ABSTRACT
The effect of continuous oestrogen treatment on uterine weight, and on cytoplasmic and nuclear oestrogen receptors was examined in rabbits. Modulation of the effects of oestrogen by progesterone was also studied. Uterine weight increased successively after exposure to oestrogen from 1 to 6 days. The concentration of both cytosolic and nuclear oestrogen receptors decreased in almost parallel fashion, however, irrespective of whether it was expressed per μg protein or μg DNA. Treatment with progesterone 5 days after oestrogenization caused no significant change in uterine weight at first. The oestrogen receptor concentration in both cytosolic and nuclear fractions decreased after 1 day but increased again after 3 days of progesterone treatment. The results indicated that there is a reduction in the actual concentration of oestrogen receptors in both cytosolic and nuclear fractions after continuous oestrogen treatment. The antagonism by progesterone of the effects produced by oestrogen appears to be transitory in nature, at least in the rabbit uterus.
J. Endocr. (1987) 115, 199–203
Effect of low temperatures on glucose-induced insulin secretion and ionic fluxes in rat pancreatic islets
Authors: Escolar J. C. , Hoo-Paris R. , Castex Ch. , Sutter B. Ch. J. 
Published: December 2008

ABSTRACT
The direct effect of cold on the inhibition of B cell secretion is well known in hibernating and experimentally hypothermic mammals. This temperature dependency may result from the inhibition of ion transport across the membranes. In order to verify this hypothesis, ionic effluxes and insulin secretion from rat islets loaded with 86Rb+ and 45Ca2+ were measured during perifusion.
At 37 °C, the rise in glucose concentration from zero to 16·7 mmol/l provoked a rapid decrease in 86Rb+ efflux, an early fall and subsequent rise in 45Ca2+ efflux and a typical biphasic pattern of insulin secretion. At 27 °C, glucose induced only a very slight increase in insulin secretion, while the fluxes of radioactive ions were not significantly modified in amplitude but were clearly delayed. At 17 °C, no insulin response to glucose was observed and the decrease in K+ conductance indicated by 86Rb+ flux decrease was less temperature-dependent than the movement of Ca2+. After supplementary stimulation with a high extracellular concentration of Ca2+, insulin secretion was enhanced at 27 °C and reached levels induced by glucose alone at 37 °C. An increase in hormone secretion occurred even at 17 °C, but only during a first phase of secretion.
Regular increases in temperature potentiated insulin secretion and provoked changes in ionic fluxes which suggest that B cell depolarization (86Rb+ flux decrease) induced by glucose can occur at 15 °C but cannot induce the opening of voltage-dependent Ca2+ channels (increase in 45Ca2+ efflux) until temperatures higher than 27 °C are reached.
These results suggest that cooling affects calcium movements especially rather than K+ conductance and insulin exocytosis per se.
J. Endocr. (1987) 115, 225–231
Effect of thyroid hormones on angiotensinogen production in the rat in vivo and in vitro
Authors: Ruiz M. , Montiel M. , Jimenez E. , Morell M. 
Published: December 2008

ABSTRACT
The influence of thyroid hormones on angiotensinogen production was studied in vitro and in vivo. In the in-vitro system, angiotensinogen production rate (APR) of monolayer cultures of rat hepatocytes in response to tri-iodothyronine (T3) and thyroxine (T4) was assayed. In the in-vivo system, plasma angiotensinogen concentration (PAC) and liver angiotensinogen content (LAC) were measured in hyper- and hypothyroid rats. In both thyroid dysfunctions, a significant decrease of PAC was found compared with that in control animals; however, LAC showed a significant increase in hyperthyroidism and a marked decrease in hypothyroidism. As PAC is dependent upon both angiotensinogen production by the liver and angiotensinogen degradation by renin, the decrease in PAC observed in hyperthyroidism could be due to an increase in plasma renin concentration, which would overcome the increased synthesis of liver angiotensinogen observed in these animals. In fact, addition of various concentrations of T4 or T3 to monolayer cultures of adult rat hepatocytes significantly enhanced APR. This increase was greater and started earlier with T3 (1196·1 ± 143·7 (s.d.) pg/mg protein per 6-h incubation; significant differences at the third hour of incubation) than with T4 (858·3 ± 88·2 pg/mg protein per 6-h incubation; significant differences at the sixth hour of incubation). In addition, a close dose–response relationship was found in the cultures supplemented with T3. The different time-course in the response elicited by T3 and T4 on APR could be a consequence of the necessary transformation of T4 into T3 to acquire biological activity.
J. Endocr. (1987) 115, 311–315
Renal vasopressin receptors in ageing C57BL/Icrfat mice
Authors: Davidson Y. S. , Davies I. , Goddard C. 
Published: December 2008

ABSTRACT
The mechanism of water conservation is impaired in ageing mammals. An age-related defect in the release of vasopressin has been implicated but, more recently, attention has moved to the renal component of the water conservation mechanism. Previous studies using renal cells prepared from mice of different ages have shown that the threshold dose of vasopressin required to elicit a significant rise in cyclic AMP (cAMP) was greater in older animals. The dose–response curve was moved to the right in 35-month-old mice, i.e. the concentration of vasopressin required to give maximum cAMP output was increased. To investigate this further we examined the binding of vasopressin to renal medullary cells maintained in short-term culture, to determine whether the decreased response of cAMP levels to vasopressin is due to changes in hormone-receptor interaction. In 6-month-old male mice the dissociation constant (Kd) was 2·38 nmol/l and the maximum binding of the hormone (Bmax) was 47·6 fmol/106 cells, and at 30 months of age Kd was 2·37 nmol/l and Bmax was 47·0 fmol/106 cells. In female mice the changes were more complicated because the data for the 6-month-old mice could be split into two groups. It is concluded that there are no age-related differences in the numbers of receptors or their affinity for vasopressin, and that the decreased cAMP response is probably associated with post-receptor mechanisms in this species.
J. Endocr. (1987) 115, 379–385
A direct action of human calcitonin gene-related peptide on isolated osteoclasts
Authors: Zaidi M. , Chambers T. J. , Das R. E. Gaines , Morris H. R. , MacIntyre I. 
Published: December 2008

ABSTRACT
The calcitonin gene encodes a small family of peptides: calcitonin, calcitonin gene-related peptide (CGRP) and katacalcin. Whereas calcitonin is concerned with skeletal maintenance, the function, if any, of katacalcin is still unknown. In the present study we have assessed resorption of human cortical bone substrate by isolated rat osteoclasts and have shown that CGRP acts directly on the osteoclast to inhibit bone resorption. The three CGRP peptides (rat, human(a) and human(β)) caused an almost equivalent decrease in osteoclastic bone resorption and were approximately 1000-fold less potent than human calcitonin in this respect. The responses of human calcitonin and human CGRP(α) were additive. Furthermore, prior treatment with trypsin to destroy receptors abolished the responsiveness of osteoclasts to CGRP and calcitonin. The carboxyl- and amino-terminal fragments of CGRP were found not to inhibit bone resorption, suggesting that the whole molecule of CGRP is necessary for biological activity. We have therefore suggested that the calcitonin-like effects of CGRP, seen both in vivo in the rat bioassay and in vitro in organ cultures, are due to the direct action of CGRP on the osteoclast, probably mediated through the calcitonin receptor. Though it is unlikely that CGRP is involved in the regulation of plasma calcium, the peptide may be an important local regulator of bone cell function.
J. Endocr. (1987) 115,511–518
Identification of multiple low molecular weight placental prolactin-like proteins produced by rat trophoblast cells
Authors: Soares M. J. , De S. K. , Foster B. A. , Julian J. A. , Glasser S. R. 
Published: December 2008

ABSTRACT
Rat trophoblast tissue was found to synthesize a number of low molecular weight proteins possessing prolactin-like characteristics. There appear to be at least three proteins that cross-react with antisera to pituitary prolactin. Two of the proteins had a molecular weight of 25 000, similar to ovine pituitary prolactin, and isoelectric points of 6·8 and 7·0. The third immunoreactive protein had a lower molecular weight (23 500), similar in size to human placental lactogen, and a slightly more acidic isoelectric point of 6·75. The molecular weight variants cross-reacted with an antipeptide serum that was generated to a synthetic peptide representing amino acids 150 to 164 of rat placental lactogen-2 (PL-2). Based on this analysis, we consider these proteins to be related to PL-2.Analysis of trophoblast proteins by gel-filtration chromatography resulted in the identification of another trophoblast prolactin. This material eluted earlier than PL-2-related proteins on a gel-filtration column, possessed prolactin-like activity (determined by competition with ovine pituitary prolactin for rabbit mammary gland or rat liver prolactin receptors) but showed limited cross-reactivity with either the antiserum to pituitary prolactin or the antiserum to the PL-2 peptide. We have thus identified multiple low molecular weight trophoblast prolactins, possessing different biochemical and immunological characteristics.
J. Endocr. (1988) 116, 101–106
Sexual maturation of male rats treated postnatally with a gonadotrophin-releasing hormone antagonist
Authors: Kolho K.-L. , Nikula H. , Huhtaniemi I. 
Published: December 2008

ABSTRACT
Postnatal secretion of gonadotrophin by male rats was inhibited by a potent gonadotrophin-releasing hormone (GnRH) antagonist analogue (N-Ac-4-Cl-d-Phe1,4-Cl-d-Phe2,d-Trp3,d-Phe6,des-Gly10-GnRH-d-alanylamide; Org 30039; 2 mg/kg s.c. twice daily) on days 1–5, 6–10, 11–15 or 16–20 of life. The onset of puberty was determined by monitoring the separation of the preputium from the glans penis, i.e. balanopreputial separation (BPS). Rats treated on days 1–5 matured normally, whereas all treatments between days 6 and 20 delayed BPS (P < 0·01). In adult rats (between 110 and 160 days of age), testis weights were reduced by 21–35% (P < 0·01) in groups treated between days 1 and 15, although weights of the accessory sex glands were normal. Testicular FSH receptors were decreased by 31–47% (P < 0·01) in all treatment groups, whereas the LH receptor content was decreased only in rats treated between days 1 and 5 (18%; P < 0·05) and prolactin receptor content decreased only in rats treated up to day 10 (31–33%; P < 0·01). Concentrations of serum testosterone, LH and FSH, and pituitary contents of LH and FSH were unaffected by neonatal treatment with Org 30039. Animals treated with Org 30039 had reduced fertility which was most pronounced (88%; P < 0·01) in rats treated between days 1 and 5. However, motile sperm were detectable in the cauda epididymis of the infertile rats.
In conclusion, postnatal gonadotrophin deprivation induced with a GnRH antagonist for different 5-day periods during the first 15 days of life delayed puberty, reduced adult testis weight and impaired fertility. Some effects of the antagonist were largely independent of the timing of gonadotrophin suppression. Other effects, including suppression of testicular LH and prolactin receptors and the delay in the onset of puberty, were found only in the younger and older treatment groups respectively. These findings emphasize the importance of neonatal hypothalamic-pituitary-gonadal function for subsequent sexual maturation.
J. Endocr. (1988) 116, 241–246
Comparison of peptide release from fetal rat hypothalamic neurones cultured in defined media and serum-containing media
Authors: Clarke M. J. O. , Gillies G. E. 
Published: December 2008

ABSTRACT
Primary cultures of rat hypothalamic neurones were maintained either in a serum-supplemented medium or in a serum-free chemically defined medium for up to 6 weeks. The release of the 41 amino acid-containing peptide, corticotrophin-releasing factor (CRF-41), vasopressin (AVP) and somatostatin (SRIF) were followed using immunoassays. In response to K+ (56 mmol/l) depolarization both the quantities of peptides released and the magnitude of responses were significantly greater from cultures maintained in the fully supplemented defined medium. As a consequence, release of CRF-41 and AVP could be measured directly, without requiring the concentration step necessary for cultures grown in serum. The response to K+ depolarization increased with the age of the culture, suggesting neuronal maturation.
Responses to K+ depolarization were Ca2+-dependent, and the addition of corticosterone (100 nmol/l) to the defined medium caused a significant reduction in the response of neurones secreting CRF-41 and AVP, but not those secreting SRIF, to depolarization. This suggests the retention in vitro of the responsiveness of stress-associated neuropeptides to the negative feedback effects of corticosterone. Neurones producing CRF-41 and AVP responded significantly in a dose-dependent manner to acetylcholine stimulation, whereas those producing SRIF did not. As cultures matured, the CRF-41- and AVP-producing neurones became more sensitive to acetylcholine with the maximal response at 1 nmol acetylcholine/1.
In conclusion, the culture of rat hypothalamic neurones is improved in terms of peptide output when the cultures are maintained in a defined medium. Differential responses of the peptidergic neurones may be seen in the presence of corticosterone and neurotransmitters, illustrating the retention in vitro of specific receptor-mediated responses which have been observed in vivo. This model should prove useful in the further study of the physiological, pharmacological and biochemical maturation and control of peptidergic neurones.
J. Endocr. (1988) 116, 349–356
Thyroid and parathyroid-independent increase in plasma 1,25-dihydroxyvitamin D during late pregnancy in the rat
Authors: Nguyen T. M. , Halhali A. , Guillozo H. , Garabedian M. , Balsan S. 
Published: December 2008

ABSTRACT
The effect of thyroparathyroidectomy (TPTX) on the plasma concentrations of the vitamin D metabolites (25-(OH)D, 24,25-(OH)2D and 1,25-(OH)2D) has been studied in pregnant rats and their fetuses during the last quarter of gestation.
Maternal and fetal vitamin D metabolites were not significantly affected by TPTX. A significant increase in plasma 1,25-(OH)2D concentrations was observed in both TPTX and control mothers and fetuses from days 19 to 21. Fetal and maternal plasma 25-(OH)D were positively correlated in both control and TPTX groups. Such a correlation was also found for 24,25-(OH)2D in the two groups. In contrast, a positive correlation between maternal and fetal plasma concentrations of 1,25-(OH)2D was found in TPTX but not in control rats.
These data suggest that major alterations in calcium metabolism, such as that produced by maternal TPTX, are insufficient to affect the changes in maternal and fetal plasma 1,25-(OH)2D during late pregnancy significantly. They also suggest that parathyroid hormone, thyroxine, and/or calcitonin may control a possible placental transfer of 1,25-(OH)2D in the rat.
J. Endocr. (1988) 116, 381–385