bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enhanced expression of transforming growth factor-β1 during thyroid hyperplasia in rats
Authors: Logan A , Smith C , Becks G P , Gonzalez A M , Phillips I D , Hill D J 
Published: December 2008

Abstract
Transforming growth factor-β1 (TGF-β1) has been reported to influence the growth rate and iodine uptake and organification in vitro by isolated thyrocytes. We have determined changes in the expression and presence of TGF-β1 within the rat thyroid during goitre induction, and subsequent involution following goitrogen withdrawal. Hyperplastic goitres were induced in adult rats by administration of methimazole together with a low iodine diet for up to 12 weeks. Goitrogen-treated rats quickly became hypothyroid compared with controls, and exhibited thyroid hyperplasia and hypertrophy assessed by thyroid weight, and DNA and protein content (control: total serum thyroxine (T4) 66 ± 4 nmol/l, thyroid weight 5 ± 1 mg/100 g body weight, mean ± s.d., n = 10; 2 weeks goitrogen: T4 undetectable, thyroid weight 27 ± 4 mg/100 g, n = 10). Thyroid growth rate slowed subsequently between 2 and 10 weeks. Messenger RNA for TGF-β1 was compared in the thyroids and livers of control and goitrous rats by ribonuclease protection assay. Low levels of mRNA for TGF-β1 were detected in thyroids from control rats at all time-points, while TGF-β1 mRNA was barely detectable in liver. Thyroid TGF-β1 mRNA levels substantially and progressively increased at 1 and 2 weeks of goitrogen treatment respectively, and remained above control levels at 4 and 10 weeks. As thyroid involution occurred 4 weeks following goitrogen withdrawal, so thyroid TGF-β1 mRNA levels declined. In control animals, the cellular localization of TGF-β1 mRNA, determined by in situ hybridization, was found to be a subpopulation of follicular epithelial cells, and immunohistochemical co-localization of TGF-β1 and calcitonin identified these tentatively as parafollicular or C-cells. During goitre formation, abundant TGF-β1 mRNA and peptide were found to be widely distributed within the entire follicular epithelium. While this ubiquitous distribution had largely disappeared in the involuting gland, TGF-β1 peptide was retained within the parafollicular cells, which appeared more abundant than in thyroids from control animals. These results suggest that an increased local expression of TGF-β1, a putative growth inhibitor, during thyroid hyperplasia may contribute to the temporal stabilization of goitre size.
Journal of Endocrinology (1994) 141, 45–57
The effect of vasopressin and oxytocin on glomerular filtration rate in the conscious rat: contribution to the natriuretic response
Authors: Forsling M L , Judah J M , Windle R J 
Published: December 2008

Abstract
Urine flow, sodium excretion, mean arterial blood pressure and glomerular filtration rate (GFR) were detennined in the conscious unrestrained rat infused with hypotonic saline. The effects of vasopressin infused at 24 and 160 pmol/min and oxytocin infused at 30 and 200 pmol/min were determined. The lower doses of each hormone gave plasma concentrations within the physiological range whereas the higher doses produced plasma concentrations equivalent to those seen following dehydration.
Vasopressin produced dose-dependent antidiuretic and natriuretic responses. Hormone infused at both rates increased the clearance of sodium, but only the higher dose caused a significant increase in GFR. Fractional excretion of sodium was significantly elevated by both doses. Oxytocin produced dose-dependent diuretic and natriuretic responses. Again both rates of infusion increased the clearance of sodium, but only the higher dose caused a significant increase in GFR. The lower dose caused a significant increase in the fractional excretion of sodium.
It appears, therefore, that increases in GFR may have a role in the natriuretic response to both hormones. However, this response can also be seen when GFR remains unchanged. This fact, together with the observed increases in the fractional excretion of sodium, indicates that these hormones have additional tubular actions.
Journal of Endocrinology (1994) 141, 59–67
The induction of hepatic somatotrophic receptors after birth in sheep is dependent on parturition-associated mechanisms
Authors: Breier B H , Ambler G R , Sauerwein H , Surus A , Gluckman P D 
Published: December 2008

Abstract
While the GH receptor (GHR) plays a key role during adult life, its role during fetal development is not well understood. Recent data suggest that GHRs are present in ovine fetal hepatic tissue at mid-gestation. However, the levels of GHR expression are markedly lower in fetal hepatic tissue in comparison with postnatal values. The present study investigates whether the neonatal induction of the hepatic GHR and plasma levels of IGF-I follow a pattern of strictly age-related development or whether birth-associated processes stimulate this increase.
Stereotaxic electrolytic lesioning of the fetal paraventricular nuclei was employed to prolong gestation markedly. We compared the hepatic binding of ovine placental lactogen (oPL) and oGH and plasma levels of IGF-I in these post-mature fetuses with those in pre-term fetuses, pregnant mothers and lambs which were of the same conceptional age as the post-mature fetuses. While specific binding of both 125I-labelled oGH and 125I-labelled oPL to hepatic microsomal membranes was fully reversible in all groups, the specific binding of 125I-labelled oGH was significantly (P<0·001) lower than specific binding of 125I-labelled oPL in all groups of animals. There was no difference in specific I-labelled oGH or 125I-labelled oPL binding in livers or plasma levels of IGF-I in post-mature fetuses in comparison with pre-term fetuses. In contrast, a major increase (P<0·001) in 125I-labelled oGH and 125I-labelled oPL binding and plasma IGF-I levels was observed in lambs. In pregnant females, specific 125I-labelled oGH and 125I-labelled oPL binding and plasma IGF-I levels were significantly (P<0·01) higher compared with the two fetal groups. A significant (P<0·001) correlation was observed between specific binding with 125I-labelled oGH and 125I-labelled oPL (r=0·95, intercept=4·5, slope=2·36). Detailed competitive binding studies showed that the potency of unlabelled oPL in competing with 125I-labelled oPL or 125I-labelled oGH was consistently higher in comparison with unlabelled oGH. The differences in cross-reactivity of oPL and oGH at the distinct developmental stages were related to the differences in affinity between the two ligands and major developmental increases in capacity.
The present study shows major parallel induction of oPL and oGH binding to hepatic microsomal membranes and plasma IGF-I concentrations after birth. The postnatal increase in the hepatic GHR is inhibited if delivery is prevented by stereotaxic destruction of the fetal paraventricular nuclei. Our observation that oGH and oPL binding is co-ordinately induced after birth in hepatic tissue supports the emerging evidence that the two ligands may bind to the same membrane receptor or to related protein(s).
Journal of Endocrinology (1994) 141, 101–108
Opioid peptide and α-adrenoceptor pathways in the regulation of the pituitary-adrenal axis in man
Authors: Delitala G , Trainer P J , Oliva O , Fanciulli G , Grossman A B 
Published: December 2008

Abstract
Opioid peptides are well established as potent inhibitors of the pituitary-adrenal axis, while α1-adrenoceptor drugs have recently been shown to stimulate this axis: both classes of agents appear to work principally above the level of the pituitary, most probable directly on the hypothalamus. There is also evidence that these drugs interact in their control of pituitary-adrenal function, although the specific hypothalamic releasing hormone involved has remained unclear. We have therefore carried out a study into the interaction of methoxamine, an α1-adrenoceptor agonist and naloxone, an opioid antagonist, together with human corticotrophin-releasing hormone (CRH), in a group of healthy volunteers in order to establish the mode of action of these drugs.
The following drugs were administered to a group of seven healthy male subjects in a randomized double-blind manner: methoxamine (6 μg/kg per min over 3 h); naloxone (10 mg bolus); human CRH (100 pg bolus); methoxamine plus CRH; naloxone plus CRH; methoxamine plus naloxone; saline (control). Plasma ACTH and serum cortisol were measured at intervals in each subject, and blood pressure and pulse rate recorded with each sample.
Both CRH and naloxone produce a marked rise in ACTH and cortisol, peaking at approximately 45 min after infusion. In combination, the drugs produced a peak response in plasma ACTH at the same time, but its magnitude was greater than that after either drug alone. Methoxamine produced a rise in plasma ACTH which was maximal at approximately 75 min, as well as a peak rise in serum cortisol at 120 min. This was greater than after either CRH or naloxone alone but, in combination, both drugs produced peak responses not significantly greater than when methoxamine alone was given.
While the interaction of drugs with differing pharmacokinetic profiles renders interpretation difficult, our data suggest that naloxone increases pituitary-adrenal activity via a mechanism independent of CRH, most probably hypothalamic vasopressin. This, albeit indirect, evidence suggests that α1-adrenoceptor activation with methoxamine activates hypothalamic pathways involving both endogenous CRH and vasopressin.
Journal of Endocrinology (1994) 141, 163–168
Effects of pituitary-gonadal suppression with a gonadotrophin-releasing hormone agonist on fetal gonadotrophin secretion, fetal gonadal development and maternal steroid secretion in the sheep
Authors: Thomas G B , McNeilly A S , Gibson F , Brooks A N 
Published: December 2008

Abstract
In order to investigate the regulation of the hypothalamo-pituitary-gonadal axis during fetal development, sheep fetuses at day 70 of gestation were implanted subcutaneously with a biodegradable implant containing the longacting gonadotrophin-releasing hormone (GnRH) agonist, buserelin. The treatment of fetuses with a GnRH agonist throughout the last half of gestation (term=145 days) abolished the increase in plasma LH concentrations that was seen in 2-day-old control lambs in response to an injection of GnRH. This attenuated response was associated with corresponding reductions in the pituitary content of LH and FSH. Immunolocalization studies revealed that pituitary glands from newborn lambs implanted with a GnRH agonist during fetal development were devoid of immunopositive LH- and FSH-containing cells. At birth the testicular weights of GnRH agonist-treated ram lambs were significantly decreased by 40% when compared with controls. This was associated with a 45% reduction in the total number of Sertoli cells per testis. In newborn ewe lambs GnRH agonist treatment had no effect on ovarian weight or on the morphological appearance of the ovaries. GnRH agonist treatment had no effect on the plasma concentrations of progesterone and oestrone in the maternal circulation or on the length of gestation. These results show (1) that GnRH positively regulates the synthesis and secretion of gonadotrophins in the fetus, (2) that reduced fetal gonadotrophic support during the last half of gestation results in a reduction in testicular growth, and (3) that fetal gonadotrophins do not affect maternal steroid secretion.
Journal of Endocrinology (1994) 141, 317–324
Characterization and localization of oxytocin receptors in the rat testis
Authors: Bathgate R A D , Sernia C 
Published: December 2008

Abstract
In this study oxytocin (OT) receptors have been characterized and localized in the testis of the rat using the radioiodinated OT receptor antagonist 125I-labelled d(CH2)5 [Tyr(Me)2,Thr4,Tyr9-NH2]-vasotocin (OTA). Receptor density and localization have been compared with the rat testis arginine vasopressin (AVP) receptor using the radioiodinated AVP V1a receptor antagonist 125I-labelled d(CH2)5Sar7-AVP and the radioiodinated linear AVP V1a antagonist 125I-labelled [(C6H5-CH2CO)-O-methyl-d-Tyr-Phe-Gln-Asn-Arg-Pro-Arg-Tyr-NH2]. 125I-labelled OTA bound with high affinity to membrane fractions of the rat testis (Ka = 13·8 ± 1·25 litres/nmol), mammary tissue (Ka=20·3± 4·36 litres/nmol) and uterus (Ka=27·8±0·74 litres/nmol). Competition studies with various OT and AVP receptor agonists and antagonists confirmed that the binding was to OT receptors. AVP receptors in the testis were found to be identical to AVP V1a receptors in the liver. The AVP receptor density in the testis was much higher than the OT receptor density (109 ±12·3 vs 5·2 ±0·79 (mean ± s.e.m.) fmol/mg protein). Autoradiographical localization showed that both OT and AVP receptors were present in the interstitial spaces in the testis consistent with binding to Leydig cells. AVP receptors were also localized on the epithelial surfaces of the seminiferous tubules and on testicular blood vessels. This study has, for the first time, found OT receptors in the testis of the rat which have similar ligand-binding characteristics to mammary and uterine OT receptors. The receptor localizations are consistent with binding to Leydig cells.
Journal of Endocrinology (1994) 141, 343–352
LH- and chorionic gonadotrophin-stimulated progesterone release in vitro by intact luteal tissue of the marmoset monkey (Callithrix jacchus)
Authors: Einspanier A , Hodges J K 
Published: December 2008

Abstract
The application of an in vitro microdialysis system (MDS) for studies on the gonadotrophic control of luteal progesterone secretion in the marmoset monkey is described. Luteal tissue collected from a total of six animals (9 ± 1 days after ovulation) was perfused with Ringer solution (without and with lipoprotein, 0·6 μg/ml). The tissue was exposed to repeated applications of human LH (hLH) and human chorionic gonadotrophin (hCG) (1, 10 and 100 IU/ml) each of 60 min duration. Perfusate was collected in 15-min fractions and assayed for progesterone content. Results showed that addition of lipoproteins to the Ringer solution had a marked effect on progesterone secretion in terms of maintaining stable baseline levels and improving reproducibility of gonadotrophin-induced responses. Progesterone secretion was significantly stimulated by both gonadotrophins at each dose tested. Maximal elevations were obtained with 10 IU/ml and there were no apparent differences in responses to hLH and hCG in terms of either magnitude or duration.
This study indicates that MDS provides a useful in vitro approach for studying the gonadotrophic control of the corpus luteum in non-human primates. The results did not demonstrate disparate actions of hLH and hCG in their ability to stimulate luteal progesterone secretion.
Journal of Endocrinology (1994) 141, 403–409
Enhancement of the granulation tissue formation in hairless mice by a potent vitamin D receptor agonist – KH 1060
Authors: Gniadecki R , Serup J 
Published: December 2008

Abstract
KH 1060 is a 20-epi analogue of 1,25-dihydroxyvitamin D3 and a potent agonist of the vitamin D receptor. Our recent finding that it stimulates glycosaminoglycan synthesis and transforming growth factor-β1 (TGF-β1) expression in normal skin provided a rationale for investigating its influence on the process of wound healing. Normal and betamethasone-impaired granulation tissue formation was studied in a polytetrafluoroethylene dead space model in hairless mice. The application of KH 1060 increased the indexes of fibroplasia and cellularity ([3H]thymidine incorporation and DNA concentration) of the betamethasone-impaired granulation tissue. Collagen production and deposition, measured as hydroxyproline synthesis and concentration in the granulation tissue, were also increased. The effect of KH 1060 on normal connective tissue repair was less pronounced; DNA and hydroxyproline concentrations in granulation tissue were unchanged. KH 1060 strongly stimulated the expression of TGF-β1 in betamethasone-impaired granulation tissue. Thus, it effectively reversed the deleterious effect of betamethasone on granulation tissue. The hyperproliferative response to this vitamin D analogue might be related to the direct stimulation of the vitamin D receptors in the granulation tissue, while the increased collagen synthesis and deposition was probably caused indirectly, via stimulation of TGF-β1.
Journal of Endocrinology (1994) 141, 411–415
Regulation of 11β-hydroxysteroid dehydrogenase activity by the hypothalamic-pituitary-adrenal axis in the rat
Authors: Walker B R , Williams B C , Edwards C R W 
Published: December 2008

Abstract
11β-Hydroxysteroid dehydrogenase (11β-OHSD) inactivates glucocorticoids and thereby modulates their access to both mineralocorticoid and glucocorticoid receptors. Since 11β-OHSD activity influences the biological responses of the hypothalamic-pituitary-adrenal axis, it might be regulated by components of this axis. We examined 11β-OHSD activity in adrenalectomized rats treated for 9 days with dexamethasone and with or without ACTH. Adrenalectomy and low-dose (2 μg/day) dexamethasone had no effect on 11β-OHSD activity in renal cortex, hippocampus or heart, and reduced enzyme activity in aorta. High-dose dexamethasone (50 μg/day) had no effect in renal cortex but increased enzyme activity by at least 50% in all other sites. This effect of dexamethasone was unaffected by the co-administration of ACTH. We also examined the metabolism of dexamethasone by 11β-OHSD in homogenized rat tissues. Only in kidney, in the presence of NAD rather than NADP, was dexamethasone converted to a more polar metabolite previously identified as 11-dehydrodexamethasone. We conclude that: dexamethasone induction of 11β-OHSD is tissue-specific, and includes vascular tissues and hippocampus but not kidney; this tissue-specificity may be explained by contrasting metabolism of dexamethasone by the isoforms of 11β-OHSD; fluctuations of glucocorticoid levels within the physiological range may not have a biologically significant effect on 11β-OHSD activity; and the inhibitory effect of ACTH, observed previously in humans, is likely to depend on the presence of intact adrenal glands.
Journal of Endocrinology (1994) 141, 467–472
Mastoparan, a wasp venom peptide, stimulates release of prolactin from cultured rat anterior pituitary cells
Authors: Mau S E , Witt M R , Vilhardt H 
Published: December 2008

Abstract
Studies have shown that mastoparan and other amphiphilic peptides induce exocytosis of hormones from anterior pituitary cells. We have studied the effect of mastoparan on the secretion of prolactin from cultured rat anterior pituitary cells and on the concomitant functional status of signal-transducing pathways in lactotroph-enriched cell cultures. Mastoparan stimulation of prolactin secretion was dose-dependent, time-dependent, reversible and required the presence of calcium. Pretreatment of pituitary cell cultures with cholera and pertussis toxin had no effect on the secretory response, whereas encapsulation of guanosine 5-[β-thio]diphosphate (GDP-β-S) by reversible electropermeabilization inhibited mastoparan-stimulated secretion. Incubation of mastoparan with myo[3H]inositol-labelled lactotroph-enriched anterior pituitary cell cultures resulted in increased formation of inositol phosphates compared with control cells, and encapsulation of GDP-β-S blocked mastoparan-induced inositol lipid hydrolysis. Mastoparan caused translocation of protein kinase C activity from a soluble to a membrane-attached form. Mastoparan was able to increase the intracellular Ca2+ concentration in Fura-2-loaded individual lactotrophs. Omission of Ca2+ from the extracellular medium did not change the Ca2+ response in lactotrophs when stimulated with mastoparan.
On the basis of these results it is concluded that mastoparan-induced release of prolactin is preceded by activation of the inositol(1,4,5)trisphosphate/diacylglycerol pathway with resulting translocation of protein kinase activity and increment in intracellular Ca2+. However, other signal-transducing pathways may be involved in the secretory process.
Journal of Endocrinology (1994) 142, 9–18
Potential role for lipoxygenase products of arachidonic acid in prostaglandin F2α-stimulated oxytocin release from the ovine corpus luteum
Authors: Cooke R G , Ahmad N 
Published: December 2008

Abstract
Intrauterine administration of nordihydroguaiaretic acid (NDGA) will maintain luteal function in sheep and also suppress the release of both oxytocin and prostaglandin F2α (PGF2α) suggesting that 5-lipoxygenase products of arachidonic acid may be involved in ovine luteolysis. During luteolysis, uterine PGF2α is considered to be the major stimulus for the secretion of luteal oxytocin, and we report the effects of 5-lipoxygenase inhibition, via intrauterine NDGA administration, on the ability of PGF2α to effect such secretion.
In the NDGA-treated ewes, luteal function was maintained and oestrus delayed, the duration of the oestrous cycle (20 ±1 days; mean ± s.d.; n=9) being significantly (P<0·01) longer than in intact controls (15 ± 1 days, n=4). Jugular infusions of PGF2α did not stimulate luteal secretion of oxytocin, the effects being comparable with those in ovariectomized ewes. In intact ewes receiving intrauterine infusions of vehicle only, PGF2α produced marked increases in luteal secretion of oxytocin. Also, preinfusion or basal concentrations of oxytocin in this group of ewes (6·6 ± 1·9 pg/ml) were significantly (P<0·01) greater than in either the NDGA-treated (3·1 ± 1·1 pg/ml) or ovariectomized (3·0 ± 0·6 pg/ml) ewes.
The results suggest involvement of 5-lipoxygenase products of arachidonic acid in the release of oxytocin from the ovine corpus luteum.
Journal of Endocrinology (1994) 142, 47–52
Effects of a polyclonal antiserum to rat growth hormone on circulating insulin-like growth factor (IGF)-I and IGF-binding protein concentrations and the growth of muscle and bone
Authors: Palmer R M , Loveridge N , Thomson B M , Mackie S C , Tonner E , Flint D J 
Published: December 2008

Abstract
A polyclonal antiserum to rat GH (anti-rGH) injected into rats for 3 or 8 weeks markedly reduced the weight, total protein and RNA content of muscles of the hind limb. These effects were prevented when bovine GH (bGH) was administered simultaneously.
In a second experiment, the effects of 8 weeks of treatment with anti-rGH on the growth of the whole body, muscle and bone were investigated. Body weights of rats were decreased by 58% by treatment with anti-rGH; muscle weights were reduced by slightly more than the decrease in body weight (by 64%, 65% and 61% respectively for plantaris, soleus and gastrocnemius). The weight of the tibia was decreased by 54%, its length was decreased by 23%, cortical width and overall width were reduced by 26% and 18% respectively, suggesting a possible role for GH in osteoclastic activity.
Serum total insulin-like growth factor-I (IGF-I) concentrations were decreased by 80–90% in both experiments by anti-rGH; these changes were prevented in the first experiment by concurrent treatment with anti-rGH and bGH. The serum IGF-binding protein-3 (IGFBP-3) concentration was also decreased by anti-rGH in experiment 1 (by 86%); the response of the 28-32 kDa IGFBPs was smaller (−35%), and was restored to control values by simultaneous injection of bGH. Western immunoblotting using an antiserum to IGFBP-2 showed that there was a marked decrease from neonatal to adult stages which was independent of anti-rGH treatment. This clearly demonstrated a dissociation of the reciprocal relationship supposed to exist between IGFBPs-2 and -3. The 24 kDa IGFBP-4 was unaffected by anti-rGH but replacement therapy with bGH doubled its concentration.
Although the effects on body and muscle weight were prevented when rats were given anti-rGH and bGH simultaneously, the possibility of mediation by other hormones cannot be precluded.
Journal of Endocrinology (1994) 142, 85–91