bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation of gill prolactin receptors in tilapia (Oreochromis niloticus) after a change in salinity or hypophysectomy
Authors: Auperin B , Rentier-Delrue F , Martial J A , Prunet P 
Published: December 2008

Abstract
Prolactin (PRL) receptors in gill tissue have been analyzed in tilapia (Oreochromis niloticus) after transfer from fresh water (FW) to brackish water (BW). This study has indicated the presence of only one class of tilapia PRL (tiPRL) receptor whatever the salinity. After transfer, however, the percentage of specific binding of the two forms of tiPRL (tiPRLI and tiPRLII) increased significantly. Scatchard analysis of tiPRLI binding indicated an increase in receptor affinity, an effect which was not accompanied by any change in receptor specificity. Transfer to BW also caused the number of tiPRL receptors to increase rapidly, remaining high in fish adapted to BW for 28 days. Based on the sharp reduction in plasma tiPRLI and tiPRLII levels after transfer to BW, one possible explanation may be that tiPRL itself is an important factor regulating the number of free receptors. This hypothesis finds support in the fact that the number of tiPRL receptors also increased in hypophysectomized fish reared in FW. However, the absence of change in receptor affinity after hypophysectomy suggested that yet other factors are involved in tiPRL receptor regulation during the transfer from FW to BW. The paradoxically high numbers of tiPRL receptors in the gills of BW-adapted tilapia, even though PRL is known to be a FW-adapting hormone, is discussed with regard to the environment in which tilapia live.
Journal of Endocrinology (1995) 145, 213–220
Effects of perinatal thyroid hormone deprivation on the growth and behaviour of newborn mice
Authors: Wallace H , Pate A , Bishop J O 
Published: December 2008

Abstract
Experiments were designed to distinguish between neonatal effects due to maternal thyroxine (T4) deprivation and those due to autonomous (fetus/pup) T4 deprivation, employing mice heterozygous for the bTG-tk transgene TG66·19 which specifically directs high-level expression of herpes virus type I thymidine kinase to the thyrocytes. Heterozygous TG66·19 females were either untreated or Ganciclovir was administered to destroy their thyrocytes and so render them T4-deficient. When mated to normal males these heterozygous females are expected to produce on average 50% normal and 50% heterozygous transgenic conceptuses. Ganciclovir was administered to the dams (both untreated and Ganciclovir-pretreated) during days 14–18 of gestation. At optimum levels of in utero Ganciclovir administration the non-transgenic pups showed no discernible effect while the transgenic pups were rendered athyrocytic and completely T4-deficient. The dams pretreated with Ganciclovir are hypothyroid throughout gestation, while the dams to which Ganciclovir was administered for the first time during gestation are not expected to become hypothyroid until about the time of parturition. In this way four sets of pups were generated for purposes of comparison: hypothyroid (transgenic) and euthyroid (non-transgenic) pups born to euthyroid dams and hypothyroid and euthyroid pups born to hypothyroid (Ganciclovir-pretreated) dams. Normal growth during days 1–10 after birth was dominated by the T4 status of the dam during gestation. Growth during days 11–21 and the correct timing of eye opening and ear elevation were dominated by the autonomous T4 status of the fetus/pup. The timely development of the surface-righting reflex (relative to weight gain) was shown to require both maternal and fetus/pup T4. The development of the cliff-avoidance reflex was independent of the T4 status of both pup and dam and of pup weight. The size of the pups at birth depended primarily on a normal T4 status in the dam but surprisingly T4 deficiency in fetuses/pups partly compensated for maternal T4 deficiency. The results presented here clearly demonstrate the utility of the HSV-tk-transgene-Ganciclovir-administration protocol in studying the interplay of maternal and fetal T4 deprivation in rodents.
Journal of Endocrinology (1995) 145, 251–262
In vivo and in vitro effects of dexamethasone on pituitary thyrotrophin-releasing hormone-like peptide concentrations in the rat
Authors: Akinsanya K O , Jamal H , Ghatei M A , Bloom S R 
Published: December 2008

Abstract
The novel peptide, pyroglutamyl-glutamyl-proline amide (pGlu-Glu-ProNH2; EEP), which has structural and immunological similarities to TRH (pGlu-His-ProNH2) has recently been shown to contribute to total TRH-like immunoreactivity (t-TRH-LI) detected in the rabbit prostate and rat and porcine anterior pituitary. In this study, the effects of dexamethasone (DEX) on rat pituitary TRH-like peptide levels in the rat were determined. TRH-like immunoreactivity (TRH-LI) was separated by ion exchange chromatography and detected by TRH RIA. Anion exchange chromatographic analysis suggested that EEP-like immunoreactivity (EEP-LI) accounted for 15·0 ± 1·2 pmol t-TRH-LI/g (70·4 ± 3·9%) in the control anterior pituitary with the remaining t-TRH-LI being due to TRH-LI.
Following DEX treatment pituitary EEP-LI and TRH-LI increased by 200% and 400% (P<0·001) respectively, constituting a 2·5-fold increase in t-TRH-LI in the pituitary. TRH-LI now accounted for 45·7±5·3% of t-TRH-LI compared with 29·6 ±4·1% in the controls. TRH-LI, but not EEP-LI, was detected in the hypothalamus and posterior pituitary, suggesting that EEP-LI is synthesised within the anterior pituitary. DEX also caused a 2·6-fold rise (P<0·001) in t-TRH-LI in dispersed, cultured anterior pituitary cells. Chromatographic analysis of cultured pituitary cell extracts revealed that the majority of t-TRH-LI (>98%) was due to TRH-LI. A possible explanation for the change in EEP-LI and TRH-LI levels in the in vivo and in vitro pituitary samples is that hypothalamic influences are necessary for the continued production of EEP-LI and are not present in vitro. Alternatively, the dissociation of the cell–cell interactions and/or the accumulation of cell products, particularly pituitary hormones in vitro, may result in a loss of the in vivo paracrine influences or the introduction of factors which inhibit EEP-LI and stimulate TRH-LI.
Journal of Endocrinology (1995) 145, 333–341
Characterization of growth hormone gene expression in the pituitary and plasma growth hormone concentrations during posthatch development in the chicken
Authors: Reiprich K , Mühlbauer E , Decuypere E , Grossmann R 
Published: December 2008

Abstract
In this study both sexes of two strains of chicken with genetically different growth potentials (broiler- and laying-type) were used to investigate growth hormone (GH) gene expression during posthatch development from day 7 (D7) to D56 by using the in situ hybridization technique and Northern analysis. In pituitaries of both strains a high GH mRNA signal was found as early as D7 by in situ hybridization, showing clear differences in the pattern of gene expression between the two strains. By Northern hybridization sex differences were detectable in all age groups of broilers, with higher levels throughout in males. In layers, however, females showed consistently higher levels compared with males until D21. While signal intensities decreased in the broiler strain during the investigation period, the layer-type strain seemed to express GH mRNA more continuously, reaching significantly (P<0·01) higher GH mRNA levels than broilers at D56. Plasma GH concentrations ran parallel to GH mRNA in early stages but showed a peak earlier at D14 and decreased after D35 in both sexes and strains. Determination of growth as weekly weight gains, however, proved that a period of rapid growth (at a higher level in both sexes of the broiler strain) at D7 was followed by a strong decrease from D14 to D21. A plateau of constant growth was reached until the end of the observation period with similar rates in both strains and sexes. Analysis of plasma thyroid hormones tri-iodothyronine/thyroxine (T3/T4) showed an increase in T3 concentrations in both strains and sexes in early stages and a decrease thereafter. No clear strain differences were measured. T4 plasma concentrations increased from D7 to D14 in broilers and D21 in layers when a plateau was reached. From the results we conclude that generally there is a good correlation between GH mRNA and plasma GH concentrations in both strains investigated. Neither parameter, however, is coupled directly with the growth rate. Thus the early rapid growth corresponds to relatively low levels of GH mRNA and plasma GH concentrations, but high T3 levels. Later, decreased growth rates are linked to increasing amounts of GH mRNA as well as increasing plasma GH concentrations in both layers and broilers. Towards the end of the observation period there was a strain divergence visible with increased amounts of GH mRNA in layers but a strong reduction in broilers. Moreover, plasma GH concentrations decreased more slowly in layers than in broilers.
Journal of Endocrinology (1995) 145, 343–353
ACTH-induced c-myc proto-oncogene expression precedes antimitogenic effect during differentiation of fetal rat adrenocortical cells
Authors: Heikkilä P , Arola J , Salmi A , Kahri A I 
Published: December 2008

Abstract
The regulation of proto-oncogenes has been connected with proliferation and differentiation in various cell types. In the present study, the ACTH-induced expression of c-myc mRNA and proliferation of fetal rat adrenocortical cells have been studied. Low levels of c-myc mRNA were detected in undifferentiated zona glomerulosa-like cells. Stimulation with ACTH for 2 to 6 h transiently increased the c-myc mRNA levels. Both basal and ACTH-induced expression levels were increased by the protein synthesis inhibitor cycloheximide. Treatment with a protein kinase C (PKC) activator 12–0-tetradecanoyl phorbol-13-acetate mimicked the effect of ACTH, whereas c-myc mRNA levels decreased by inhibiting the PKC with H-7. ACTH inhibited proliferation of fetal rat adrenocortical cells during the first 24 h of stimulation. The inhibitory effect began from 6 h, reached its maximum at 12 h and slowly vanished at 24 h.
Our data demonstrated that ACTH transiently increased c-myc mRNA expression. Adrenocortical c-myc expression was mediated via PKC. In contrast to previous reports, where c-myc expression precedes proliferation of various cells, ACTH-induced c-myc mRNA expression of cultured fetal rat adrenocortical cells was followed by inhibition of proliferation.
Journal of Endocrinology (1995) 145, 379–385
Luminal glucagon-like peptide-1(7–36) amide-releasing factors in the isolated vascularly perfused rat colon
Authors: Plaisancié P , Dumoulin V , Chayvialle J-A , Cuber J-C 
Published: December 2008

Abstract
Glucagon-like peptide-1 (GLP-1) is released from endocrine cells of the distal part of the gut after ingestion of a meal. GLP-1 secretion is, in part, under the control of hormonal and/or neural mechanisms. However, stimulation of the colonic L cells may also occur directly by the luminal contents. This was examined in the present study, using an isolated vascularly perfused rat colon. GLP-1 immunoreactivity was measured in the portal effluent after luminal infusion of a variety of compounds which are found in colonic contents (nutrients, fibers, bile acids, short-chain fatty acids (SCFAs)). Oleic acid (100 mm) or a mixture of amino acids (total concentration 250 mm), or starch (0·5%, w/v) did not increase GLP-1 secretion over basal value. A pharmacological concentration of glucose (250 mm) elicited a marked release of GLP-1 which was maximal at the end of infusion (400% of basal), while 5 mm glucose was without effect on secretion. Pectin evoked a dose-dependent release of GLP-1 over the range 0·1–0·5% (w/v) with a maximal response at 360% of basal when 0·5% pectin was infused. Cellulose or gum arabic (0·5%) did not modify GLP-1 secretion. The SCFAs acetate, propionate or butyrate (5, 20 and 100 mm) did not induce a significant release of GLP-1. Among the four bile acids tested, namely taurocholate, cholate, deoxycholate and hyodeoxycholate, the last one was the most potent at eliciting a GLP-1 response with a maximal release at 300% and 400% of the basal value when 2 and 20 mm bile acid were administered respectively. In conclusion, some fibres and bile acids are capable of releasing colonic GLP-1 in rats and may contribute to the secretory activity of colonic L cells.
Journal of Endocrinology (1995) 145, 521–526
Differences in carbohydrate composition of FSH preparations detected with lectin-ELISA systems
Authors: Rafferty B , Mower J A , Ward H L , Rose M 
Published: December 2008

Abstract
FSH is a glycoprotein containing N-linked carbohydrates which exhibit a variety of forms ranging from mono- to multibranched structures. Variation in glycosylation, particularly the degree of terminal sialylation, determines the half-life of the hormone and hence its in vivo bioactivity. The glycoform content of FSH preparations can differ according to the source (e.g. pituitary, urine), cell line (for rDNA-derived material) and selectivity of purification procedures, and may create difficulties in the preparation and characterization of standards and therapeutic products. In order to develop a simple method to detect changes in glycocomposition, an FSH ELISA was modified by the incorporation of lectins of recognized sugar specificity, and used to examine the terminal sugar composition of ampouled preparations of pituitary, urinary and rDNA-derived FSH.
FSH was captured with a specific monoclonal antibody (MAb) and detected with either biotinylated anti-FSH MAb (ELISA) or the sugar-specific lectins (L-ELISA) from Triticum vulgaris (sialic acid, SA), Sambucus nigra (α2,6-linked SA), Maackia amurensis (α2,3-linked SA) or Ricinus communis (free terminal galactose; GAL). Relative estimates of the amounts of terminal SA, its different forms and GAL were derived from the L-ELISA/ELISA data compared with the highly sialylated 1st International Standard for pituitary FSH (IS) 83/575.
All the FSH preparations had less SA than the IS with the ratio of α2,3- and α2,6-linked SA varying between preparations. The amounts of α2,6-linked SA relative to the IS were not significantly different in the urinary and pituitary preparations whereas α2,3-linked SA in all preparations was generally less than that of the standard. The rDNA FSH material, produced in CHO cells, was confirmed as containing only α2,3-linked SA. The degree of asialylation revealed by the Ricinus lectin showed that the more heavily sialylated IS had less exposed GAL than the other preparations. The method provides a simple and rapid technique for assessing changes in terminal sugar composition and allows comparison of the patterns of terminal glycosylation between preparations from different sources and, when assayed against the appropriate standard, between batches of therapeutic products.
Journal of Endocrinology (1995) 145, 527–533
Developmental regulation of androgen receptor in rat ovary
Authors: Tetsuka M , Whitelaw P F , Bremner W J , Millar M R , Smyth C D , Hillier S G 
Published: December 2008

Abstract
Androgen receptor (AR) distribution and developmental regulation in the rat ovary were examined by semiquantitative immunohistochemistry. Ovarian AR mRNA levels were also determined by Northern analysis of total RNA and compared with the levels of cytochrome P450aromatase (P450arom), an established marker of preovulatory follicular maturity. Hypophysectomized immature female rats were treated with recombinant human (rh)-FSH and/or rh-LH, or human menopausal gonadotrophin (HMG). AR was predominately located in granulosa cells. There was no indication of specific AR immunoreactivity in thecal cells, but scattered stromal cells did stain positively. In control and LH-treated ovaries, only small preantral/early antral follicles were present. Granulosa cells in these follicles showed intense AR immunostaining. Treatment with FSH, FSH and LH or HMG stimulated varying degrees of preovulatory follicular development. In these follicles, the intensity of AR immunostaining progressively declined as follicular development progressed. In intact immature rats treated with FSH, the abundance of ovarian AR mRNA was significantly decreased to 35% of the control value while combined treatment of FSH and LH resulted in further down-regulation of AR mRNA expression to 17% of the control value. A decrease in the abundance of AR mRNA was accompanied by a simultaneous increase in the abundance of P450arom mRNA. Similar results were obtained in hypophysectomized immature rats treated with FSH and LH, suggesting an inverse relationship between AR mRNA expression and granulosa cell maturity. These results suggest that (1) the AR is most abundant in the granulosa cells of rat ovaries and (2) the expression of AR and its mRNA are developmentally regulated, being down-regulated during FSH-stimulated preovulatory follicular development.
Journal of Endocrinology (1995) 145, 535–543
Circulating insulin-like growth factors (IGFs), IGF-binding proteins (IGFBPs) and tissue mRNA levels of IGFBP-2 and IGFBP-4 in the ovine fetus
Authors: Carr J M , Owens J A , Grant P A , Walton P E , Owens P C , Wallace J C 
Published: December 2008

Abstract
The IGF-binding proteins (IGFBPs) are a family of at least six structurally related proteins, which bind the IGFs and modulate their actions, including the regulation of preand postnatal growth. In this study we have examined the relationship between circulating and tissue mRNA levels of IGFBPs and related this to circulating IGFs in the fetal sheep over the gestational period when rapid growth and development occurs. Circulating IGFBP-2, as measured by Western ligand blot (WLB), increases between early and mid gestation, remains high, then declines throughout late gestation (P=0·0002). Circulating IGFBP-3 increases throughout gestation, as measured by WLB or RIA (P=0·04 and P=0·0001 respectively), as does circulating IGFBP-4 (P=0·004). These ontogenic changes in circulating IGFBPs-2 and -4 are paralleled by changes in liver mRNA for these proteins and, for IGFBP-2, by those in kidney IGFBP-2 mRNA also. This suggests that liver and kidney may be the primary contributors to circulating IGFBP-2 and the liver to circulating IGFBP-4. IGFBP-2 mRNA is present in the heart and lung in early gestation but barely detectable in these tissues after approximately 60 days gestation. IGFBP-4 mRNA is also present in the heart in early but not late gestation, but is abundant in the lung throughout gestation. These results demonstrate tissue specific and developmental regulation of IGFBPs-2 and -4 at the mRNA level. To assess any role the circulating IGFs may play in mediating these changes in IGFBPs, or vice versa, both plasma IGF-I and IGF-II were measured by RIA. Circulating IGF-I increases as gestation progresses (P=0·0001), while circulating IGF-II increases between early and mid gestation, remains high (P=0·01), then declines. Circulating IGF-I is positively correlated with fetal weight (r=0·66, P=0·03), circulating IGFBP-3 (r=0·54, P=0·01) and IGFBP-4 (r=0·52, P=0·01). Circulating IGF-II positively correlates with circulating IGFBP-2 (r=0·48, P=0·02) throughout gestation and at 1 day postnatally. These relationships are consistent with circulating IGF-I influencing IGFBPs-3 and -4, and similarly, IGF-II determining IGFBP-2, or vice versa. Alternatively, these correlations may reflect coordinate regulation of IGF and IGFBP by a common factor.
Journal of Endocrinology (1995) 145, 545–557
Effects of ovarian steroids on hypothalamic opioid receptor subtypes in ovariectomized ewes: regional changes in density and affinity
Authors: Shen P J , Smith A I , Evans R G , Clarke I J 
Published: December 2008

Abstract
The negative feedback regulation by ovarian steroids of luteinizing hormone secretion may be partially mediated by a hypothalamic endogenous opioid mechanism. This could be affected by ovarian steroid-regulated changes in hypothalamic opioid receptor binding mechanisms. In this report we show that in the presence of blocking concentrations of site-selective opioid analogues, [3H]diprenorphin homogeneously labelled μ, δ or κ receptor subtypes respectively. Using this receptor binding model, we characterized each opioid receptor subtype in the hypothalamic preoptic area and medio-basal hypothalamus of ovariectomized (OVX) and OVX plus progesterone- or oestradiol-17β (OE2)-treated ewes. In the preoptic area, progesterone treatment did not influence the affinity or capacity of δ or κ receptor binding sites, but significantly reduced μ receptor subtype content (20% less than control) with no statistically significant change in affinity. There was no effect of OE2 on either the affinity or capacity of each opioid receptor subtype in this area. In the mediobasal hypothalamus, progesterone treatment significantly decreased δ subtype receptor affinity (22 ± 11 nm vs control 7 ± 2 nm) and increased binding capacity (78 ± 9 fmol/mg protein vs control 37 ± 16 fmol/mg protein). OE2 treatment had a similar, though more profound effect on affinity (51 ± 17 nm) and binding capacity (139 ± 26 fmol/mg protein) at the δ receptor binding site. There were no significant changes in the affinity or capacity of μ or κ binding sites in the medio-basal hypothalamus. These results indicate that steroid hormones modulate hypothalamic opioid receptors in the OVX ewe in a receptor subtype- and region-dependent manner. The precise role of these steroid-induced changes in opioid receptor characteristics remains to be determined.
Journal of Endocrinology (1995) 145, 559–567
Relative roles of the thyroid hormones and noradrenaline on the thermogenic activity of brown adipose tissue in the rat
Authors: Cageao L F , Noli M I , Mignone I R , Farber M , Ricci C R , Hagmüller K , Zaninovich A A 
Published: December 2008

Abstract
We have assessed the relative contribution of the thyroid hormones and noradrenaline (NA) on the calorigenic function of brown adipose tissue (BAT) as indicated by GDP binding and O2 consumption of BAT mitochondria. Male Wistar rats of 200 g body weight were made hypothyroid with 131I. Groups of animals were injected s.c., in divided doses, daily for 10 days, with thyroxine (2 μg/100 g body weight) or tri-iodothyronine (T3; 0·3 μg/100 g body weight). Animals were used 7 days after bilateral or unilateral sympathetic nerve excision of BAT (Sx). Sham-operated rats were used as controls. In normal rats kept at 22 °C, GDP binding reached 94 ± 24 pmol/mg protein; untreated hypothyroid rats had normal binding values whereas the T3-treated group showed an increased binding. Sx induced a sharp fall in the three groups (P<0·01). After 24-h exposure to 4 °C GDP binding increased in normal rats to about 410% (P<0·01) whereas binding failed to increase in response to cold in the untreated hypothyroid and the T3-treated groups. Sx reduced GDP binding in the three groups significantly (P<0·01). The consumption of O2 by BAT mitochondria showed similar variations in response to Sx and to cold exposure as did GDP binding. The data indicated that, at room temperature, BAT calorigenesis can function without the thyroid hormones, though not without the catecholamines. The findings in rats exposed to cold showed that the lack of NA was significantly more effective than the lack of thyroid hormones in preventing the BAT hyperactive response. This does not negate an active role for T3 in BAT calorigenesis.
Journal of Endocrinology (1995) 145, 579–584