bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of insulin-like growth factor-I peptides in rats with acute renal failure
Authors: Martin A A , Gillespie C M , Moore L , Ballard F J , Read L C 
Published: December 2008

Abstract
The effect of insulin-like growth factor-I (IGF-I) administration on body weight gain and the rate of recovery of renal function was investigated in rats following an acute episode of renal ischaemia. Since the des(1–3)IGF-I and LR3IGF-I variant forms of IGF-I have been shown to be more potent than IGF-I, their effects were also examined. Acute renal failure was produced in male Sprague–Dawley rats by clamping both renal arteries for 45 min. Treatment was commenced at the time of renal artery occlusion with vehicle (0·1 mol acetic acid/l; control group), IGF-I (2·0 mg/kg per day), des(1–3)IGF-I (2·0 mg/kg per day) or LR3IGF-I (1·5 mg/kg per day) by s.c. osmotic pump, and continued for 7 days, with rats being held in metabolism cages. Glomerular filtration rate (GFR) was estimated by the use of 51Cr-EDTA continuously infused i.p. via osmotic pump. Following the episode of renal ischaemia, body weight gain and nitrogen retention were significantly improved in all three peptide-treated groups, and serum urea concentrations were reduced in the groups treated with IGF-I and des(1–3)IGF-I. However, there was no evidence of the variants having any increased potency over the growth effects of IGF-I itself. GFR was significantly reduced, urine output was increased and urinary concentrating ability was reduced in all groups compared with normal rats, with no significant effect of the IGF peptides being apparent.
A closer examination of the acute effects of LR3IGF-I on renal function was undertaken by measuring GFR for 3 days before and 3 days after renal ischaemia in two groups of rats, treated for the latter 3 days with either vehicle (controls) or LR3IGF-I (1·5 mg/kg per day). LR3IGF-I treatment following renal ischaemia resulted in a significantly greater fall in GFR than in controls, urinary osmolality was also significantly reduced, and fractional excretion of sodium was increased. In addition, there was histological evidence of a greater degree of tubular epithelial calcification in the kidneys of the rats treated with LR3IGF-I.
This study showed that administration of IGF peptides at doses sufficient to cause significant improvement in anabolic status did not improve renal function in rats following an acute episode of renal ischaemia. Indeed the LR3IGF-I variant of IGF-I had a deleterious effect on renal function in the early stage of the recovery period.
Journal of Endocrinology (1994) 140, 23–32
The role of neuropeptides in the regulation of adrenal zona glomerulosa function: effects of substance P, neuropeptide Y, neurotensin, Met-enkephalin, Leu-enkephalin and corticotrophin-releasing hormone on aldosterone secretion in the intact perfused rat adrenal
Authors: Hinson J P , Cameron L A , Purbrick A , Kapas S 
Published: December 2008

Abstract
A range of neuropeptides has been identified in the adrenal glands of many mammalian species. In many cases these peptides have been located in nerves supplying the adrenal cortical cells, or within clusters of chromaffin cells within the zona glomerulosa. The function of these neuropeptides has yet to be determined, but from their location within the gland it is clearly possible that they may have a role in the regulation of aldosterone secretion. The effects of Met-enkephalin, Leu-enkephalin, neuropeptide Y, substance P, corticotrophin-releasing hormone (CRH) and neurotensin on aldosterone secretion were investigated using the intact perfused rat adrenal gland in situ. All the peptides tested, except CRH, caused a significant increase in aldosterone secretion over the dose range of 1 pmol to lOnmol, with a maximum response of about a twofold increase in secretion. Met-enkephalin, however, at a dose of 10 nmol caused a 350% increase in aldosterone secretion, a response comparable with that seen in response to angiotensin II in this preparation. These results suggest that, while substance P, neuropeptide Y, neurotensin and Leu-enkephalin all have the capacity to cause modest increases in the rate of steroid secretion by the zona glomerulosa, these neuropeptides probably do not have a major role in the acute regulation of aldosterone secretion, at least under basal conditions. Met-enkephalin, on the other hand, was a more potent stimulus to aldosterone secretion, and thus may have a role in the control of aldosterone secretion.
Journal of Endocrinology (1994) 140, 91–96
FSH and LH up-regulate epidermal growth factor receptors in rat granulosa cells
Authors: Fujinaga H , Yamoto M , Shikone T , Nakano R 
Published: December 2008

Abstract
Epidermal growth factor (EGF) modulates ovarian folliculogenesis and steroidogenesis and its binding sites have been demonstrated in the ovary. We investigated the localization of EGF-binding sites in the rat ovary, and the effects of FSH and LH on EGF binding to cultured granulosa cells. Autoradiographic localization of 125I-labelled mouse EGF-binding sites was demonstrated in the granulosa and luteal cells. Displacement study and Scatchard analysis showed that a single class of specific binding sites for 125I-labelled mouse EGF was present in the granulosa cells, obtained from the ovaries of immature rats treated with diethylstilboesterol. The number of binding sites and the apparent dissociation constant were 4336 binding sites/cell and 3·42 pmol/l respectively. The granulosa cells were cultured for 48 h at 37 °C in medium alone or with increasing amounts of ovine FSH (oFSH; 1–1000 μg/l). FSH treatment increased 125I-labelled mouse EGF binding to the granulosa cells in a dose-dependent manner. After culture with oFSH (100 μg/l) for 48 h, the cells were cultured in medium alone or with increasing amounts of ovine LH (oLH; 1–1000 μg/l) for an additional 48 h. LH treatment also increased 125I-labelled mouse EGF binding in a dose-dependent manner, compared with the control. However, neither FSH nor LH altered receptor-binding affinity. Furthermore, after culture with oFSH (FSH-primed) or oFSH followed by oLH (LH-primed), tissue plasminogen activator (tPA) activities in the conditioned media were examined by fibrin autography. FSH-primed or LH-primed granulosa cells were more responsive to EGF action to induce an increase in tPA activity. In conclusion, it is suggested that functional receptors for EGF in rat granulosa cells are up-regulated by FSH and LH.
Journal of Endocrinology (1994) 140, 171–177
In situ localization of muscle insulin-like growth factor-II mRNA in developing bovine fetuses
Authors: Listrat A , Gerrard D E , Boulle N , Groyer A , Robelin J 
Published: December 2008

Abstract
Insulin-like growth factor-II (IGF-II) modulates myogenesis in muscle cell cultures, in utero. IGF-II gene expression is developmentally regulated in several tissues including muscle. Determining whether IGF-II is expressed by developing muscle cells or by neighbouring cells in developing muscle tissue is crucial for determining whether IGF-II exerts a paracrine or an autocrine affect on myogenesis. Semitendinosus muscle samples from 12 bovine fetuses ranging from 60 to 274 days post conception (pc) were analysed for the amount and localization of muscle IGF-II mRNA using Northern, dot blot and in situ hybridization analyses. Northern blot analysis revealed multiple IGF-II transcripts of 5·1, 3·7, 2·6, 2·0, 1·7 and 1·1 kb in developing bovine muscle tissue. The relative amount of muscle IGF-II mRNA increased (P<0·05) until 162 days pc, then decreased (P<0·01) to near undetectable levels by the end of gestation (approximately 284 days pc). Between 60 and 162 days pc, in situ hybridization revealed that the majority of the IGF-II transcripts were localized to developing muscle cells rather than connective tissue. After 162 days pc the IGF-II hybridization signal shifted away from muscle cells and greater accumulation was observed in the connective tissue at 274 days pc. These data confirm that the expression of IGF-II in developing bovine muscle tissue is primarily localized in muscle cells and support the claim that IGF-II acts as an autocrineacting growth factor during myogenesis in vivo.
Journal of Endocrinology (1994) 140, 179–187
Growth hormone but not gonadal steroids influence lipoprotein lipase and hepatic lipase activity in hypophysectomized rats
Authors: Vikman-Adolfsson K , Oscarsson J , Nilsson-Ehle P , Edén S 
Published: December 2008

Abstract
Lipoprotein lipase and hepatic lipase are involved in the degradation and cellular uptake of lipids in peripheral tissues and the liver. These enzymes seem to be influenced by gonadal steroids in the rat as well as in man. Since gonadal steroids have been shown to influence the secretory pattern of GH and since the effect of gonadal steroids on several metabolic functions may be dependent upon their effects on GH secretion, the present study was undertaken to investigate the developmental regulation of heparin-releasable lipoprotein lipase and hepatic lipase activities in female and male rats, and to study the effects of gonadal steroids and different modes of GH administration to hypophysectomized rats on these enzyme activities. Female and male Sprague–Dawley rats from 20 to 65 days of age were studied. Hypophysectomy was performed at 50 days of age and these rats were given replacement therapy with thyroxine and cortisone. Groups of hypophysectomized rats were treated with either oestradiol valerate (0·1 mg/kg per day) or testosterone enanthate (1 mg/kg per day). Bovine GH (1 mg/kg per day) was given to groups of hypophysectomized rats either by two daily subcutaneous injections or by continuous infusion using osmotic minipumps. Hormone treatment was given for 1 week. Lipoprotein lipase and hepatic lipase activities were measured in heparinized plasma.
There was no difference in lipoprotein lipase activity between male and female rats at 20 to 45 days of age. Lipoprotein lipase activity decreased between 45 and 65 days of age in male rats but not in females and, at 65 days of age, lipoprotein lipase activity was higher in females compared with males. Hepatic lipase activity increased from 20 to 45 days of age in both female and male rats but at 45 and 65 days of age it was higher in female than in male rats. Hypophysectomy decreased lipoprotein lipase and hepatic lipase activity in female rats. Neither oestradiol nor testosterone treatment had any effects in hypophysectomized rats. Treatment with bovine GH increased both lipoprotein lipase and hepatic lipase activities irrespective of its mode of administration and these effects were not influenced by additional treatment with oestradiol or testosterone. After the last injection of GH, lipoprotein lipase activity was increased for 12 h. Hepatic lipase activity was increased at 2 and 4 h after the last GH injection but after 12 h the activity had decreased, indicating that the time-course for the effects of GH on lipoprotein lipase and hepatic lipase may be different.
It is concluded that GH markedly influences post-heparin lipoprotein lipase and hepatic lipase activities. The lack of effects of gonadal steroids on these activities in hypophysectomized rats suggests that the gonadal steroids influence these lipases via their influence on GH release.
Journal of Endocrinology (1994) 140, 203–209
Effect of thyroidectomy, and thyroxine and α2u-globulin replacement therapy on testicular steroidogenic and gametogenic activities in rats
Authors: Biswas N M , Ghosh P K , Biswas R , Ghosh D 
Published: December 2008

Abstract
Adult male rats were thyroidectomized and killed after 22 days of treatment. Thyroidectomy lowered the weights of testes and accessory sex organs, decreased the activities of testicular Δ5-3β- and 17β-hydroxysteroid dehydrogenases (HSD), and diminished spermatogenesis, serum levels of testosterone and α2u-globulin. Supplementation with thyroxine at a dose of 5 μg/100 g body weight per day for 21 days or supplementation with α2u-globulin at a dose of 1·5 mg/rat per day for 21 days in thyroidectomized animals partially reversed the decrease in HSD activities and serum concentrations of testosterone and α2u-globulin, while spermatogenesis was restored to normal. The weights of testes and accessory sex organs were also reinstated after supplementation with thyroxine or α2u-globulin in thyroidectomized rats in comparison with thyroidectomized animals. It was concluded that α2u-globulin may be an intermediary in the thyroid hormone control of testicular function.
Journal of Endocrinology (1994) 140, 343–347
Developmental changes in and hormonal modulation of epidermal growth factor concentration in the rat submandibular gland
Authors: Hiramatsu M , Kashimata M , Takayama F , Minami N 
Published: December 2008

Abstract
Developmental changes in and hormonal effects on the concentration of epidermal growth factor (EGF) in the rat submandibular gland were investigated. The level of EGF in the gland gradually increased with age from 4 up to 8 weeks of age; thereafter it increased markedly, reaching a plateau level at 12 weeks of age in both male and female rats. A significant sex difference in EGF levels was observed between 8 and 14 weeks, the level in the males being approximately twice as high as that in the females at 12 and 14 weeks of age. Castration of male rats decreased EGF to about the same level as that of control females. Treatment of castrated rats with testosterone propionate (TP) restored EGF to the levels in control male rats. Ovariectomy and/or administration of oestradiol-17β to ovariectomized rats had no apparent effect on EGF concentration. These findings indicate that the sex difference in EGF concentration can be attributed to the level of endogenous androgens. In addition, hypophysectomy of male rats caused a remarkable decrease in submandibular gland EGF to about 7% of the normal level. This reduction was significantly, although not completely, restored by the administration of TP, tri-iodothyronine (T3) or GH. Moreover, giving TP with T3 or with GH or both together had additive effects on the increase in EGF levels in hypophysectomized rats. These results provide evidence that EGF in the submandibular gland is regulated multi-hormonally by at least TP, T3 and GH.
Journal of Endocrinology (1994) 140, 357–363
Plasma concentration of atrial natriuretic peptide and brain natriuretic peptide during normal human pregnancy and the postpartum period
Authors: Yoshimura T , Yoshimura M , Yasue H , Ito M , Okamura H , Mukoyama M , Nakao K 
Published: December 2008

Abstract
Increases in blood volume are observed during normal gestation and these are reversed shortly after delivery. Although both atrial (A-type) natriuretic peptide (ANP) and brain (B-type) natriuretic peptide (BNP) have been described, the role of these peptides in pregnancy and the postpartum period are unclear. This study was designed to examine the effects of pregnancy, labour and delivery on plasma levels of ANP and BNP. Plasma levels of ANP and BNP were determined during normal pregnancy, 30 min after separation of the placenta (immediately postpartum) and between 5 and 72 h postpartum (late postpartum; puerperium). Since the assay sensitivity was 20 pg/ml plasma (for both ANP and BNP), values less than this were assigned a value of 20 pg/ml to calculate means. Plasma levels of ANP and BNP were significantly higher at term pregnancy than during the first trimester (ANP increased from 20 ± 0·2 to 57 ± 10 pg/ml (s.e.m.), P<0·001; BNP increased from 25 ± 2 to 49 ± 9 pg/ml, P<0·01). The plasma level of ANP then rose to 157 ± 38 pg/ml 30 min after separation of the placenta, being significantly (P<0·01) higher than that seen at term pregnancy. It declined significantly (P<0·001) to 32 ± 3 pg/ml in the late postpartum period. In contrast, the plasma level of BNP 30 min after separation of the placenta was 80 ± 25 pg/ml, and increased to 116 ± 17 pg/ml in the late postpartum period, significantly (P<0·01) higher than the level at term pregnancy. We conclude that ANP and BNP may play a role in controlling blood volume during normal human pregnancy at term and during transition to the postpartum period. Changes in ANP immediately postpartum and BNP in the later postpartum period appear to be differentially regulated.
Journal of Endocrinology (1994) 140, 393–397
Inhibition of growth hormone bioactivity by recombinant human growth hormone-binding protein in the eluted stain assay system
Authors: Dattani M T , Hindmarsh P C , Brook C G D , Robinson I C A F , Marshall N J 
Published: December 2008

Abstract
The effects of a recombinant human GH-binding protein (rhGHBP; amino acids 1–238) on GH stimulation of rat Nb2 lymphoma cells were examined with an eluted stain assay system (ESTA). This precise bioassay utilizes the colorimetric reduction by stimulated Nb2 cells of a yellow tetrazolium salt (3-[4,5-dimethyl-thiazol-2-yl]-2,5-diphenyl-tetrazolium bromide) to a purple formazan as its end-point. The use of a lactogenic bioassay allowed the investigation of hGHBP specificity for human GH (hGH) as opposed to prolactin. rhGHBP inhibited pituitary hGH bioactivity in a dose-dependent manner. No significant inhibition of prolactin or ACTH bioactivity occurred. It was confirmed that recombinant 20 kDa hGH also stimulated the Nb2 cells and that its relative potency was ∼ 10% of that of pituitary-derived hGH. Stimulation by 20 kDa hGH was also inhibited by rhGHBP. The highly quantitative ESTA system demonstrated that the binding protein inhibited in a competitive manner. hGH activation of the Nb2 cells did not appear to be governed by a Michaelian first-order reaction. As might then be anticipated, the concentration of rhGHBP required for 50% inhibition of GH bioactivity (IC50) changed with agonist concentrations for both 20 kDa and 22 kDa hGH. However, with equimolar concentrations of these two isohormones, the IC50 of the binding protein was virtually identical. Potentiation of hGH bioactivity in vivo by low concentrations of hGHBP has been reported but was not observed in our in vitro system when tested over a wide range of binding protein concentrations.
In conclusion, the ESTA bioassay system permitted a detailed characterization of the inhibition of hGH bioactivity by rhGHBP. The hormonal specificity confirms earlier radioligand binding studies, except that we found that the 20 kDa hGH variant interacts with the rhGHBP.
Journal of Endocrinology (1994) 140, 445–453
Effect of chronic exposure to a gonadotrophin-releasing hormone agonist on in vitro responsiveness of ovine pituitary cells to inhibin, activin and oestradiol
Authors: Muttukrishna S , Knight P G 
Published: December 2008

Abstract
To investigate the extent to which the direct actions of inhibin, activin and oestradiol on pituitary output of FSH and LH are dependent on the presence of functional gonadotrophin-releasing hormone (GnRH) receptors, we have compared the effects of these agents on cultured ovine pituitary cells derived from control and GnRH agonist-suppressed ewes.
Chronic treatment with GnRH agonist reduced plasma LH and FSH levels (P<0·01) and abolished GnRH-induced release of LH and FSH both in vivo and in vitro. As expected, basal LH release and LH cell content in vitro were drastically reduced in GnRH agonist-suppressed cells (P<0·001). However, basal FSH release and FSH cell content were approximately twofold higher than in control cells (P<0·001).
Irrespective of whether the cells had been desensitized to GnRH, inhibin and oestradiol were both found to suppress basal FSH release and FSH cell content in a dose-dependent fashion (P<0·001). Although inhibin had no effect on basal release of LH from control cells, it markedly enhanced GnRH-induced release (P<0·001). In contrast, inhibin increased (P<0·001) basal LH release from GnRH agonist-suppressed cells (which were unresponsive to the GnRH challenge). Inhibin had no overall effect on total LH content/well for either control or GnRH agonist-suppressed cells. Treatment with oestradiol, on the other hand, reduced total LH content/well, an effect which was more pronounced with GnRH agonist-suppressed cells (−44%; P<0·001) than with control cells (−14%, P<0·01). Whereas in control cells activin had no significant effect on any aspect of FSH production examined, in GnRH agonist-treated cells activin enhanced basal FSH release, residual cell content and total FSH content/well (P<0·001). Altering GnRH receptor status also modified the LH response to activin. With control cells activin increased basal release (P<0·001), decreased GnRH-induced release (P<0·001) and increased total LH content/well (P<0·001). With GnRH agonist-treated cells, however, activin had a uniform inhibitory effect on each aspect of LH production examined (P<0·001 in each case).
It was concluded that desensitization of ovine gonadotrophs to GnRH by chronic agonist treatment results in a paradoxical enhancement of FSH output in vitro but has little effect on the responsiveness of the cells (in terms of gonadotrophin release and content) to either inhibin or oestradiol. In contrast, GnRH agonist treatment leads to qualitative changes in cellular reponsiveness to activin.
Journal of Endocrinology (1994) 140, 483–493
Evidence for a role of phospholipase A2 in the mechanism of LHRH priming in rat anterior pituitary tissue
Authors: Thomson F J , Johnson M S , Mitchell R , Wolbers B 
Published: December 2008

Abstract
The phospholipase A2 (PLA2) inhibitors, quinacrine, p-bromophenacyl bromide, ONO-RS-082, aristolochic acid and chloracysine blocked the priming effect of LHRH, but not acute LHRH-induced gonadotrophin release measured in anterior pituitary pieces in pro-oestrous rats in vitro. These results suggest that the intracellular mechanisms underlying LHRH priming are distinct from those which mediate LH release in the present circumstances in that they involve PLA2. Furthermore, neither LHRH-induced LH release from preprimed tissue nor Ca2+-induced LH release were attenuated by quinacrine, indicating that this inhibitor does not interfere with the general Ca2+-dependent secretory apparatus of the gonadotroph and that the critical period for its action is in the induction of priming. LHRH induced the release of [3H]arachidonic acid ([3H]AA) from [3H]AA-prelabelled anterior pituitary tissue from pro-oestrous rats; a response which was sensitive to inhibitors of PLA2, of protein kinase C (PKC) and of protein synthesis. Activation of PKC also resulted in [3H]AA release which was inhibited with exactly the same pharmacological profile as the response to LHRH. Both gonadotrophin secretion and [3H]AA release responses to LHRH and to phorbol ester varied in parallel during the oestrous cycle and in ovariectomized/oestradiol-17β-replaced animals, as did their sensitivity to quinacrine and the protein synthesis inhibitor cycloheximide. These results indicate that LHRH priming is dependent on a hormonally regulated cascade involving a distinct form of PKC acting through a protein synthesis-dependent step to release AA by means of PLA2 activity. The priming effect was mimicked (at least in part) by conditioning preincubation with AA, confirming the functional relevance of this signalling cascade. Results using standard inhibitors of lipoxygenase/epoxygenase pathways were equivocal as to whether these pathways were critically involved, whilst cyclo-oxygenase inhibitors were completely without effect. The steps downstream from AA (and its possible metabolites) by which stimulus–secretion coupling is up-regulated in priming remain to be clarified.
Journal of Endocrinology (1994) 141, 15–31