bluuebunny/crossref_metadata_2025_split huggingface dataset:
Growth hormone control of tissue protein metabolism in dwarf mice: enhancement by a monoclonal antibody
Authors: Bates P. C. , Aston R. , Holder A. T. 
Published: December 2008

ABSTRACT
Monoclonal antibody (MAb) to GH has been shown to increase the anabolic response induced by the hormone in individual tissues of dwarf mice. Dwarf mice were treated with GH at a low and a high dose (2·5 and 50 mU/day respectively), with and without complexing to an MAb. Treatment was for 7 and 14 days, at which times protein synthesis rates in skeletal muscle, liver and heart were determined from incorporation of labelled phenylalanine following injection of a flooding dose. The MAb potentiated the actions of GH and produced increases in the rates of protein synthesis in each of the tissues to a significantly greater extent than did GH alone.
The increase in protein synthesis rate induced by MAb appears to be mechanistically distinct from that observed by increasing the dose of GH. In skeletal muscle and liver there was a dose–response to the GH alone in terms of the RNA concentration, i.e. the capacity for protein synthesis, whereas in each tissue examined the MAb caused very little further response in the RNA concentration. The MAb-induced enhancement of protein synthesis rate was almost entirely due to an increase in the RNA activity, i.e. the efficiency of the synthesizing system.
Complexing GH to a particular MAb, or to antisera of restricted epitope specificity, has previously been shown to enhance the in-vivo effects of GH on whole body protein content; the mechanism for this enhancement has not been adequately determined. The present results suggest that the mechanism of MAb enhancement of GH activity is unlikely to be through prolonging GH action by increasing its serum half-life, but may be through effects on GH-receptor response, possibly through targeting of the GH to a particular receptor sub-type or through inhibition of internalization of the GH-receptor complex.
Journal of Endocrinology (1992) 132, 369–375
Involvement of physiological prolactin levels in growth and prolactin receptor content of prostate glands and testes in developing male rats
Authors: Pérez-Villamil B. , Bordiú E. , Puente-Cueva M. 
Published: December 2008

ABSTRACT
We have investigated the role of physiological prolactin levels in the development of prepubertal male rats. Prolactin GH and testosterone levels, as well as body, ventral prostate and testicular weight, have been analysed in both control and bromocriptine-treated rats between 21 and 60 days of life. Furthermore the role of prolactin in the regulation of its own receptors has also been studied during the same period. In control rats, prolactin levels showed a prepubertal peak of secretion at 25 days of age. At this time GH and testosterone levels were low and did not show any significant variation. After this age, prolactin levels increased more gradually; determinations of GH showed great variation with low levels in most of the rats and very high values in the other animals; testosterone levels remained low until day 35 after which they increased. Simultaneously with the serum prolactin peak on day 25, a decrease in prolactin-binding capacity of ventral prostate glands, was observed and a maximum rate of body, prostate and testicular weight gain was obtained. Furthermore, in rats with pharmacologically suppressed serum prolactin levels (lower than 1 μg/l), prolactin binding to prostate glands as well as the weight of body, ventral prostate and testes were lower than in control animals. When results were expressed in mg prostate or testes/g body weight, testes from 25-day-old treated rats weighed significantly less than controls. The later stages of development, from days 25 to 60, were characterized by an initial decline in serum prolactin levels at 29 days of age which was followed by a continuous increase until adult values were reached. During this period, prostatic prolactin receptors which were at their lowest value at 33 days of age showed a gradual rise parallel with the observed increase in plasma prolactin levels. When testicular tissue was analysed, no changes in prolactin-binding sites caused by sexual maturation were observed. The present results indicate that physiological prolactin secretion has a specific effect on the normal increase in the prostate, testes and body weight and clearly is also implicated in the regulation of its prostatic receptors at the earlier stages of development.
Journal of Endocrinology (1992) 132, 449–459
Thyrotrophin receptors in normal and neoplastic (primary and metastatic) canine thyroid tissue
Authors: Verschueren C. P. , Rutteman G. R. , Vos J. H. , Van Dijk J. E. , de Bruin T. W. A. 
Published: December 2008

ABSTRACT
Thyrotrophin (TSH) is the conditional growth factor of thyroid epithelial cells. Abnormalities in TSH-receptor binding such as a low receptor number or low binding affinity may be a marker of thyroid carcinoma or metastases, or may exhibit a relationship with the functional variability of such tissues. The dog was used as a model to characterize TSH-receptor binding in normal thyroid tissues, naturally occurring thyroid neoplasms and distant metastases. In normal dog thyroid tissues, specific 125I-labelled TSH binding ranged from 2·7 to 15·5%, and low cross-reactivity with bovine LH (0·023%) was observed. One class of TSH-binding sites was found in eight normal thyroid tissues and 22 thyroid carcinomas; two normal thyroid tissues and one tumour exhibited two classes of binding sites. The concentration of binding sites was lower in the five carcinomas with reduced pertechnetate uptake (0·09 pmol/mg protein) than in the five thyroid neoplasms with increased uptake (0·19 pmol/mg) (P= 0·055). Compared with the original carcinoma tissues, TSH binding revealed a reduced binding affinity in eight out of eleven metastases. Two metastases showed a complete absence of TSH binding, suggesting that they were not dependent on TSH for growth. We conclude that one class of TSH-binding site is predominant in normal dog thyroid tissues and dog thyroid carcinomas. TSH could therefore contribute, at least in theory, to further growth of primary dog thyroid carcinomas. Secondly, assays measuring TSH binding may not be able to discriminate between malignant and benign dog thyroid tumours. TSH receptor number or affinity may be related to the functional variability of thyroid neoplasms. The absence of TSH binding in some metastases demonstrated that this characteristic can be acquired during the natural history of a differentiated thyroid carcinoma.
Journal of Endocrinology (1992) 132, 461–468
Modification of the amounts of G proteins and of the activity of adenylyl cyclase in human benign thyroid tumours
Authors: Delemer B. , Dib K. , Patey M. , Jacquemin C. , Corrèze C. 
Published: December 2008

ABSTRACT
The possibility that a TSH post-receptor-binding defect is responsible for the pathogenesis of benign thyroid tumours was studied. Thus, we attempted to determine in hyperfunctioning (hot) nodules and non-functioning (cold) nodules whether the functional activity or the amount of G proteins were modified in comparison with surrounding normal tissues. The adenylyl cyclase response to agonists that bypass the TSH–receptor complex (forskolin, guanosine 5′- (β.γ-imido)triphosphate (Gpp(NH)p) or [A1F4]−) was studied on membranes from tumorous and adjacent normal thyroid tissues. We also examined the ability of G proteins to be ADP-ribosylated by cholera toxin (CT) or pertussis toxin (PT), and quantified G proteins by Western blot analysis with specific antisera directed against Gsα and Giα subunits.
Basal adenylyl cyclase activity was unchanged in hot tumours compared with normal tissue whereas the stimulation of adenylyl cyclase by Gpp(NH)p or [A1F4]− (which act directly on Gs) as well as by forskolin (which acts on the catalyst) was significantly (P<0·05) decreased in five of seven nodules studied. Two types of response were found in cold nodules, depending upon whether they were microfollicular or macrofollicular tumours. Basal as well as stimulated adenylyl cyclase activity was increased (0·02<P<0·05) in microfollicular tumours. In contrast, in macrofollicular tumours basal adenylyl cyclase was unchanged whereas stimulated adenylyl cyclase activity was decreased (0·02<P<0·05). The ability of Gs or Gi to be ADP-ribosylated by CT or PT respectively was maintained in tumorous tissue. Quantification of Gs revealed a 30% decrease (P<0·05) in the level of Gs in hot tumours and either an increase or a decrease in cold tumours compared with their respective normal tissue. Quantitative or qualitative changes in Gi protein were also observed, but there was no clear difference between the patients with hot and cold thyroid tumours. A decrease or an increase in adenylyl cyclase activity can therefore be explained by an alteration in the amounts of G proteins, at least in some benign thyroid tumours.
Journal of Endocrinology (1992) 132, 477–485
INTERLEUKIN-1 AND INTERLEUKIN-6 IN BREAST CYST FLUID: THEIR ROLE IN REGULATING AROMATASE ACTIVITY IN BREAST CANCER CELLS
Authors: Reed M.J. , Coldham N.G. , Patel S.R. , Ghilchik M.W. , James V.H.T. 
Published: December 2008

ABSTRACT
Gross cystic breast disease is a common benign disease which may be associated with an increased risk for breast cancer. Breast cyst fluid (BCF) contains many steroids, peptide growth factors and proteins. We have now identified interleukin-1 (IL-1) and IL-6 in BCF by specific radioimmunoassays. Concentrations of IL-1 were similar in BCF with low or high Na+/K+ ratios (ratio <3 vs >3; 357 ± 72 pg/ml vs 308 ± 126 pg/ml). In contrast, IL-6 concentrations were significantly higher (P<0.01) in BCF with a Na+/K+ ratio >3 (2.75 ± 2.34 ng/ml) compared with BCF with a low electrolyte ratio (0.21 ± 0.09 ng/ ml). BCF (10%, v/v) stimulated aromatase activity when added to dexamethasone stimulated breast tumour-derived fibroblasts and there was a significant correlation between the stimulation of aromatase activity and BCF Na+/K+ ratio (r = 0.95, P<0.001). A significant correlation was also found between stimulation of aromatase activity and concentration of IL-6 in BCF (r = 0.80, P<0.01) but not IL-1 concentration (r = −0.39, not significant). Addition of IL-1 or IL-6 (50 ng/ml) to fibroblasts stimulated aromatase activity but was associated with a small (20%) decrease in cell growth. It is concluded that IL-6 may have an important role in regulating aromatase activity in breast cancer cells.
Possible mechanisms for reduction of circulating concentrations of progesterone by interferon-α in cows: effects on hyperthermia, luteal cells, metabolism of progesterone and secretion of LH
Authors: Barros C. M. , Betts J. G. , Thatcher W. W. , Hansen P. J. 
Published: December 2008

ABSTRACT
Experiments were performed to determine the mechanism by which recombinant bovine interferon-αI1 (rbIFN-α) causes an acute reduction in plasma concentrations of progesterone. In experiment 1, administration of a prostaglandin synthesis inhibitor blocked rbIFN-α-induced hyperthermia but did not prevent the decline in plasma concentrations of progesterone. The decline in progesterone concentrations caused by rbIFN-α was, therefore, not a direct consequence of the associated hyperthermia or of pathways mediated through prostaglandin synthesis. It is also unlikely that rbIFN-α acts to increase the clearance of progesterone since injection of rbIFN-α did not decrease plasma concentrations of progesterone in ovariectomized cows given an intravaginal implant of progesterone (experiment 2). In experiment 3, rbIFN-α did not affect basal and LH-induced release of progesterone from cultured luteal slices, indicating that rbIFN-α is unlikely to affect luteal function directly. Injection of rbIFN-α did, however, cause a decrease in plasma concentrations of LH in ovariectomized cows (experiment 4) that coincided temporally with the decrease in progesterone concentrations seen in cows having a functional corpus luteum. The present results strongly suggest that rbIFN-α acts to reduce secretion of progesterone by interfering with pituitary support for luteal synthesis of progesterone. The finding that rbIFN-α can inhibit LH secretion implies that interferon-α molecules should be considered among the cytokines that can regulate hypothalamic or pituitary function.
Journal of Endocrinology (1992) 133, 175–182
The anabolic effect of 17β-oestradiol on the trabecular bone of adult rats is suppressed by indomethacin
Authors: Chow J. W. M. , Lean J. M. , Abe T. , Chambers T. J. 
Published: December 2008

ABSTRACT
We have previously demonstrated that administration of oestrogen, at doses sufficient to raise serum concentrations to those seen in late pregnancy, increases trabecular bone formation in the metaphysis of adult rats. To determine whether prostaglandins (PGs), which have been shown to induce osteogenesis in vivo, play a role in the induction of bone formation by oestrogen, 13-week-old female rats were given daily doses of 4 mg 17β-oestradiol (OE2)/kg for 17 days, alone or with indomethacin (1 mg/kg). The rats were also given double fluorochrome labels and at the end of the experiment tibias were subjected to histomorphometric assessment. Treatment with OE2 suppressed longitudinal bone growth and increased uterine wet weight, as expected, and neither response was affected by indomethacin. Oestrogen also induced a threefold increase in trabecular bone formation in the proximal tibial metaphysis, which resulted in a substantial increase in trabecular bone volume. As previously observed, the increase in bone formation was predominantly due to an increase in osteoblast recruitment (as judged by an increase in the percentage of bone surface showing double fluorochrome labels), with only a minor increase in the activity of mature osteoblasts (as judged by the mineral apposition rate). Indomethacin abolished the increase in osteoblastic recruitment, but the activity of mature osteoblastic cells remained high. The bone formation rate and bone volume remained similar to controls. The results suggest that PG production may be necessary for the increased osteoblastic recruitment induced by oestrogen, but not to mediate the effects of oestrogen on the activity of mature osteoblasts.
Journal of Endocrinology (1992) 133, 189–195
Vasoactive intestinal peptide stimulation of aldosterone secretion by the rat adrenal cortex may be mediated by the local release of catecholamines
Authors: Hinson J. P. , Kapas S. , Orford C. D. , Vinson G. P. 
Published: December 2008

ABSTRACT
The effects of vasoactive intestinal peptide (VIP) on adrenocortical function were investigated using several different preparations of adrenocortical tissue. VIP caused a significant increase in perfusion medium flow rate and in aldosterone and corticosterone secretion by the isolated perfused rat adrenal gland, with a threshold of 1 pmol in 200 μl, but did not affect basal steroid secretion by collagenase-dispersed adrenocortical cells at any concentration used, from 10 pmol/l to 10 μmol/l. The presence of VIP (100 nmol/l) had no significant effect on the response of zona glomerulosa cells to stimulation by ACTH at any concentration. In incubations of intact adrenal capsular tissue, VIP (10 μmol/l) caused a significant stimulation of aldosterone secretion, and also induced a significant release of adrenaline into the incubation medium. Addition of (−)alprenolol (100 nmol/l), a βadrenergic antagonist, to the incubation medium significantly attenuated the response of capsular tissue to VIP. It is concluded that the effects of VIP on aldosterone, which are only seen when the architecture of the zona glomerulosa is preserved, may be mediated by the local release of adrenaline.
Journal of Endocrinology (1992) 133, 253–258
Daily rhythms in the hormone content of the neurohypophysial system and release of oxytocin and vasopressin in the male rat: effect of constant light
Authors: Windle R. J. , Forsling M. L. , Guzek J. W. 
Published: December 2008

ABSTRACT
Patterns of neurohypophysial hormone secretion and changes in the hormone content of the hypothalamus and posterior pituitary lobe were monitored in the male rat for cycles of 24 h in association with changes in food and water intake and fluid excretion. Plasma oxytocin and vasopressin concentrations were seen to rise significantly over the hours of daylight, decreasing during the night. Parallel changes were seen in the immunoreactive material in the hypothalamus, whilst the content of the neurohypophysis was inversely related to plasma concentrations. The ratio of plasma oxytocin:vasopressin reached a significant peak at about 02.00 h which might be related to the feeding activity of the rats, food and water intake being largely confined to the night, as was fluid excretion. On exposure to constant light, despite initial disruption hormonal rhythms were still seen but showed a phase shift. The relationships between plasma and tissue levels were maintained. Patterns of food and water intake and urinary excretion were little affected by exposure to constant light, remaining largely confined to the former night phase. The hormonal rhythms appeared to be more closely related to the activity of the rats, which also showed a phase shift during constant light.
Journal of Endocrinology (1992) 133, 283–290
Phosphate transport by fibroblasts from patients with hypophosphataemic vitamin D-resistant rickets
Authors: Escoubet B. , Silve C. , Balsan S. , Amiel C. 
Published: December 2008

ABSTRACT
It is accepted that renal phosphate wasting is the basis of hypophosphataemia in vitamin D-resistant hypophosphataemic rickets (VDRR). Abnormal renal adaptation to phosphate deprivation has also been reported in these patients. We studied sodium-dependent phosphate transport and its modulation by phosphate deprivation in skin fibroblasts cultured from healthy subjects and patients with VDRR. Control fibroblasts exhibited high-affinity sodium-dependent phosphate transport (77 ± 12 μmol/l) which resembled the ubiquitous transport of renal and non-renal cells. Phosphate deprivation (incubation in low phosphate medium) increased the maximal velocity (Vmax) of the transport by 2·7-fold after 24 h, with no change in the affinity. The increase in Vmax was dependent on gene transcription and protein synthesis. The sodium-dependent phosphate transport exhibited in fibroblasts from VDRR patients did not significantly differ from that of control subjects, except that the Vmax of the phosphate transport was higher in cells from patients with VDRR under normal and phosphate-deprivation conditions, although the difference was significant only after 24 h of phosphate deprivation (Vmax: 22·6 ± 2·4 pmol/mg protein per s in VDRR vs 16 ± 3·6 pmol/mg protein per s in controls, P < 0·05).
These data demonstrate that sodium-coupled phosphate transport in human skin fibroblasts has the properties of ubiquitous sodium-phosphate co-transport and show that this transport is not deficient in patients with VDRR. Indeed paradoxically the Vmax was 40% higher in VDRR than in control subjects after 24 h of phosphate deprivation. The transport must be either different from that of kidney cells responsible for the phosphate leak, or differently modulated. Therefore, skin fibroblasts cannot be used to determine the molecular defect responsible for the renal phosphate leak in VDRR patients.
Journal of Endocrinology (1992) 133, 301–309
Tri-iodothyronine stimulates rat osteoclastic bone resorption by an indirect effect
Authors: Allain T. J. , Chambers T. J. , Flanagan A. M. , McGregor A. M. 
Published: December 2008

ABSTRACT
Tri-iodothyronine (T3) increases bone resorption in vivo and in vitro. In order to understand further the mechanisms by which this occurs we studied the effects of T3 at concentrations in the range of 1 pmol/l–1 μmol/l on bone resorption by osteoclasts isolated from neonatal rat long bones. Osteoclasts were disaggregated and incubated either with or without UMR 106 cells or with mixed bone cells. We found that there was no effect of T3 on bone resorption by osteoclasts incubated alone or co-cultured with UMR 106 cells. However, in culture with mixed bone cells there was a significant relationship between the concentration of T3 and bone resorption (r = 0·54, P= 0·01) The greatest effect was observed at a T3 concentration of 1 μmol/l at which a 1·8-fold increase in resorption was seen compared with control (P <0·005; paired t-test). We conclude that the ability of T3 to increase osteoclastic bone resorption is not due to a direct action of T3 on osteoclasts but is mediated by another cell present in bone. The observation that UMR 106 cells are unable to mediate this effect suggests that either the mediating cell is not osteoblastic or the phenotype of UMR 106 does not conform to the phenotype of osteoblastic cells that mediate the T3 responsiveness of bone.
Journal of Endocrinology (1992) 133, 327–331
Expression and translation of the growth hormone-receptor gene in the guinea-pig
Authors: Harvey S. , Fraser R. A. 
Published: December 2008

ABSTRACT
The refractoriness of guinea-pigs to the growth-promoting actions of exogenous GH has been suggested to be due to a deficiency or defect in tissue GH receptors or in GH-receptor gene expression. GH-receptor mRNA was, however, demonstrated by Northern blot analysis and by the polymerase chain reaction in extracts of guinea-pig liver, adipose tissue, brain, hypothalamus and pituitary gland. High-affinity, low-capacity binding sites for radio-labelled ovine GH were also demonstrated on the plasma membranes of guinea-pig liver and were similar to those in rat liver. These results demonstrate that the unresponsiveness of guinea-pigs to exogenous GH is not due to the absence of GH receptors.
Journal of Endocrinology (1992) 133, 357–362
The effects of hypo- and hyperthyroidism on fibre composition and mitochondrial enzyme activities in rat skeletal muscle
Authors: Lomax R. B. , Robertson W. R. 
Published: December 2008

ABSTRACT
Hypo- and hyperthyroidism have been associated with changes in the activities of mitochondrial enzymes in homogenates of skeletal muscles, but it is unclear whether such changes were due to changes in single fibre enzyme activities or to previously documented changes in relative numbers of fibres. In this study the activities of the mitochondrial enzymes α-glycerol phosphate dehydrogenase (m-αGPDH) and succinate dehydrogenase (SDH) were measured in single fibres of the soleus and gastrocnemius muscles of the rat by cytochemical assays.
In the soleus muscles of hypothyroid animals there was a decrease in the mean percentage (± s.d.) of type II fibres from 8·0 ± 6·0 to 0·8 ± 1·9% (P < 0·05) and decreases in SDH activities in all fibre types (P < 0·005). In the gastrocnemius muscles of these animals there were no changes in fibre composition but type IIB fibres had reduced (P < 0·05) m-αGPDH activities. In the hyperthyroid animals, in which body weight had increased relative to the euthyroid animals, there were increases in the percentages of type IC and type II fibres in the soleus from 4·3 ± 1·7 to 13·1 – 9·0% (P < 0·05) and from 9·6 ± 7·2 to 33·4 ± 9·6% (P < 0·005) respectively and an increase in the percentage of type IIA fibres in the gastrocnemius from 92·9 ± 2·3 to 97·0 ± 2·9% (P < 0·05). However, there were no increases in single fibre mitochondrial enzyme activities. It is therefore suggested that the administration of moderate, growth-promoting doses of thyroid hormones to euthyroid animals can cause changes in muscle fibre composition without stimulating the activities of mitochondrial enzymes.
Journal of Endocrinology (1992) 133, 375–380