bluuebunny/crossref_metadata_2025_split huggingface dataset:
Involvement of protein kinase C in the stimulation of sodium-dependent phosphate transport by parathyroid hormone in osteoblast-like cells
Authors: Arao Makoto , Yamaguchi Toru , Sugimoto Toshitsugu , Fukase Masaaki , Chihara Kazuo 
Published: December 2008

Arao M, Yamaguchi T, Sugimoto T, Fukase M, Chihara K. Involvement of protein kinase C in sodiumdependent phosphate transport by parathyroid hormone in osteoblast-like cells. Eur J Endocrinol 1994;131:646–51. ISSN 0804–4643
The rat osteosarcoma cell line UMR-106 has an osteoblast-like phenotype and possesses parathyroid hormone (PTH)-responsive dual signal transduction systems [adenosine 3′,5′-cyclic monophosphatedependent protein kinase (PKA) and calcium-protein kinase C (Ca-PKC)]. These cells transport inorganic phosphate (Pi) by a Na+-dependent carrier under stimulation by PTH. The present study aimed to clarify PTH-responsive signal transduction mechanisms in the regulation of Na+-dependent Pi transport by PTH in UMR-106 cells. Exposure of these cells to 10−7 mol/l PTH induced a significant increase in Pi uptake within 30 min of incubation and it became maximal after 2 h. Parathyroid hormone (10−9 –10−7 mol/l) stimulated Pi uptake dose dependently. Activation of PKC by 12-O-tetradecanoyl phorbol- 13-acetate (TPA) also increased Pi uptake in time- and dose-dependent manners similar to PTH In contrast, neither PKA activation by 10 mol/l forskolin or by 10−4 mol/l dibutyryladenosine 3′,5′-cyclic monophosphate nor calcium ionophore treatment with 10−7 mol/l A23187 or with 10−7 mol/l ionomycin during 3-h incubations affect Pi uptake, except its increase by 10−4 mol/l forskolin at a 3-h incubation. These agents had no influence on Pi uptake even in combined treatments with TPA. The PTH-induced increase in Pi uptake was abolished almost completely by pretreating cells with PKC inhibitors, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride (H-7) (50 μmol/l) or staurosporin (10 and 50 nmol/l), and by down-regulating PKC with a prolonged TPA treatment. These results indicate that the messenger system mediated by PKC, rather than by PKA or by cytosolic calcium, plays a crucial role in the regulation of Na+-dependent Pi transport by PTH within a few hours of exposure of the hormone in the osteoblast-like cells.
Toru Yamaguchi, Third Division, Department of Medicine, Kobe University School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650, Japan
Neuroendocrine regulation of growth hormone
Authors: Bertherat Jérôme , Bluet-Pajot Marie Thérèse , Epelbaum Jacques 
Published: December 2008

Bertherat J, Bluet-Pajot MT, Epelbaum J. Neuroendocrine regulation of growth hormone. Eur J Endocrinol 1995;132:12–24. ISSN 0804–4643
This short review is focused on the neuroendocrine regulation of growth hormone (GH) pulsatile secretory pattern and GH gene expression. The neuronal network involved in the central control of GH includes extrahypothalamic neurons such as the noradrenergic and cholinergic systems, which regulate the two antagonistic neurohormonal systems: somatostatin (SRIH) and GH-releasing hormone (GHRH). Intrahypothalamic Proopiomelanocortin- and Galanin-containing interneurons also participate in the regulation of SRIH and GHRH neuronal activity, which also is dependent on sex steroids and GH and/or insulin-like growth factor I (IGF-I) feedback. cAMP (controlled mainly by GHRH and SRIH), thyroid and glucocorticoid hormones, IGF-I and activin are among the factors that regulate GH gene expression at the transcriptional level and may play a role in somatotroph differentiation and proliferation during ontogeny as well as physiological and pathological states such as acromegaly.
J Epelbaum, U159 INSERM, Centre Paul Broca, 2 ter rue d'Alésia, 75014 Paris, France
Quadriceps and hand-grip strength in adults with childhood-onset growth hormone deficiency
Authors: Sartorio Alessandro , Narici Marco , Conti Antonio , Monzani Marco , Faglia Giovanni 
Published: December 2008

Sartorio A, Narici M, Conti A, Monzani M, Faglia G. Quadriceps and hand-grip strength in adults with childhood-onset growth hormone deficiency. Eur J Endocrinol 1995;132:37–41. ISSN 0804–4643
The effects of chronic growth hormone (GH) deficiency on muscle size and strength of postural (quadriceps) and non-postural (hand-grip) muscle groups, as well as on vertical jump capacity, were evaluated in six adults with childhood-onset GH deficiency. Data obtained were compared to those recorded in an age-, sex- and exercise-matched healthy control group. Thigh muscle plus bone cross-sectional area (CSAM+B) of the dominant quadriceps was significantly lower (p < 0.001) than in controls, while the CSAM+B/Body height)2 ratio was similar to that of controls. The maximum voluntary contraction (MVC) of the quadriceps of patients was significantly lower (p < 0.002) than in controls, while no differences existed in the quadriceps force expressed per unit area (MVC/CSA) between patients and controls. As far as hand-grip was concerned, the CSAM+B of the dominant forearm was significantly lower (p < 0.003) than in controls, while the CSAM+B/Body height)2 ratio was no different. The hand-grip MVC of patients was significantly lower (p < 0.004) than in controls, while no differences existed in the MVC/CSA ratio. It is noteworthy also that no difference existed in the hand-grip to quadriceps MVC ratio of the two groups. Furthermore, no differences were found in the vertical jump capacity, because both Δ Height and Δ Height/Body weight of patients were not significantly different from those of controls. In conclusion, our study suggests that GH deficiency seems to reduce the size and strength of postural and non-postural muscle groups to the same extent. However, these findings are likely to be attributed to a simple dimensional scaling, because their CSA/ (Body height)2, MVC/CSA and vertical jump capacity were comparable to those of controls.
Alessandro Sartorio, Laboratorio Sperimentale di Ricerche Endocrinologiche, Centro Auxologico Italiano, IRCCS, via Ariosto 13, 1-20145 Milan, Italy
Bone turnover and bone mineral density in young adult patients with panhypopituitarism before and after long-term growth hormone therapy
Authors: Balducci Rina , Toscano Vincenzo , Pasquino Anna M , Mangiantini Adele , Municchi Giovanna , Armenise Patrizia , Terracina Sandra , Prossomariti Giancarlo , Boscherini Brunetto 
Published: December 2008

Balducci R, Toscano V, Pasquino AM, Mangiantini A, Municchi G, Armenise P, Terracina S, Prossomariti G, Boscherini B. Bone turnover and bone mineral density in young adult partients with panhypopituitarism before and after long-term growth hormone therapy. Eur J Endocrinol 1995;132:42–6. ISSN 0804–4643
We examined the effects of biosynthetic growth hormone (GH) on biochemical indices of bone turnover and on bone mineral density in a group of GH-deficient adults. Thirteen patients (eight males and five females) aged 24 ± 5 years (range 16–35) were studied before and 12 and 24 months after GH treatment (0.1 IU, kg− day−1, 6 days a week). Serum levels of insulin-like growth factor I (IGF-I), calcitonin, parathyroid hormone, alkaline phosphatase, intact osteocalcin, fasting urinary hydroxyproline/creatinine ratio and bone mineral density (BMD), measured at the lumbar spine by dualphoton absorptiometry, were evaluated. After 12 months of treatment, IGF-I, alkaline phosphatase, osteocalcin and the fasting urinary hydroxyproline/creatinine ratio increased significantly. However, after 24 months of therapy, serum levels of osteocalcin decreased to pretreatment values while IGF-I, fasting urinary hydroxyproline/creatinine ratio and alkaline phosphatase remained elevated significantly. No changes were found in parathyroid hormone and calcitonin plasma levels or in BMD either after 12 or 24 months of treatment. These data demonstrate that GH, at the dosage that we used, activates bone turnover during 24 months of therapy in adults with panhypopituitarism, even if a downward trend for osteocalcin became apparent at 24 months. However, this activation in bone turnover was not accompanied by an increase in BMD. We can hypothesize that GH, at the relatively high dosage used, may stimulate osteoclastic activity to a greater extent than osteoblastic activity. It is probable that the dose of GH replacement therapy in adults plays a key role
R Balducci, Dipartimento di Sanita Pubblica, Universita "Tor Vergata", Via di Tor Vergata 38, 00173 Roma, Italy
Abnormal calcitonin basal levels and pentagastrin response in patients with chronic renal failure on maintenance hemodialysis
Authors: Niccoli Patricia , Brunet Philippe , Roubicek Christa , Roux François , Baudin Eric , Lejeune Pierre-Jean , Berland Yvon , Conte-Devolx Bernard 
Published: December 2008

Niccoli P, Brunet P, Roubicek C, Roux F, Baudin E, Lejeune P-J, Berland Y, Conte-Devolx B. Abnormal calcitonin basal levels and pentagastrin response in patients with chronic renal failure on maintenance hemodialysis. Eur J Endocrinol 1995;132:75–81. ISSN 0804–4643
Hypercalcitoninemia has been reported in renal failure. Using a specific monomeric calcitonin (CT) immunoassay, we measured CT levels in 154 hemodialyzed patients. The relationship between CT and serum intact parathyroid hormone (PTH), gastrin, alkaline phosphatases, phosphate and calcium was studied. The pentagastrin test was performed in 26 patients exhibiting basal hypercalcitoninemia. Basal CT levels over 5.7 pmol/l (20 ng/l) were found in 25.3% of the patients and values higher than 26 pmol/l (90 ng/l) in 7.8%. Although CT is cleared by hemodialysis, post-dialysis CT levels either were unchanged or increased as compared with pre-dialysis values. This suggests that hypercalcitoninemia is not related to a decreased renal clearance, and that hemodialysis induces a specific regulatory pathway. None of the parameters studied were found to explain high CT levels. Of the patients with hypercalcitoninemia, 11.5% exhibited abnormal CT response to pentagastrin but no relationship between CT and phosphate, calcium and PTH levels was evidenced. Our findings confirm high CT monomer levels in renal failure. As there was no correlation with parameters classically involved in CT regulation, its physiological significance remains unclear. Abnormal CT response to pentagastrin raises the problem of its specificity as a tumoral marker with regard to medullary thyroid carcinoma.
B Conte-Devolx, Service d'Endocrinologie et Maladies Métaboliques, Hôpital de la Conception, 147 Bd Baille, Marseille 13385 cedex 05, France
Immunohistochemical localization of inhibin α- and βA-subunits in the ovary of immature female rats
Authors: Kobayashi Mitsuko , Yamoto Mareo , Minami Sawako , Imai Miyako , Nakano Ryosuke 
Published: December 2008

Kobayashi M, Yamoto M, Minami S, Imai M, Nakano R. Immunohistochemical localization of inhibin α- and βA-subunits in the ovary of immature female rats. Eur J Endocrinol 1995;132:97–102. ISSN 0804–4643.
Immunohistochemical localization of inhibin α- and βA-subunits was examined in the ovaries of immature female rats. The granulosa cells in various sized ovarian follicles obtained from rats that were 10–24 days old exhibited positive staining for inhibin α- and βA-subunits. The relative intensities of immunostaining for α- and βA-subunits increased during follicular growth and maturation. Ova and internal thecal cells did not show any immunostaining for inhibin α- and/or βA-subunits. These results suggest that granulosa cells of immature rat ovaries may produce inhibin from the 10th day after birth, and that an increase in the number of mature ovarian follicles results in an increase in inhibin production in the immature rat ovary during prepubertal development.
Mitsuko Kobayashi, Department of Obstetrics and Gynaecology, Wakayama Medical College, 1 shichibancho, Wakayama 640, Japan
Pituitary–testicular axis in rats lacking testicular macrophages
Authors: Gaytan F , Bellido C , Aguilar E , van Rooijen N 
Published: December 2008

Gaytan F, Bellido C, Aguilar E, van Rooijen N. Pituitary–testicular axis in rats lacking testicular macrophages. Eur J Endocrinol 1995;132:218–22. ISSN 0804–4643
Testicular macrophages were depleted selectively in adult rats by intratesticular injections of liposome-entrapped dichloromethylene diphosphonate (Cl2MDP-lp), whereas control animals received intratesticular injections of phosphate-buffered saline-containing liposomes or 0.9% NaCl. The absence of macrophages in Cl2MDP-lp-injected rats was confirmed histologically. Rats lacking testicular macrophages showed significantly increased (twofold on average) serum concentrations of luteinizing hormone at 5 and 10 days after treatment. Serum luteinizing hormone concentrations drop to control values at 15 days after treatment. Serum testosterone concentrations were increased significantly (twofold on average) at 5, 10 and 15 days after treatment. No significant changes were found for follicle-stimulating hormone serum concentrations, or for the weights of the testes and sex accessory organs. Testicular histology was unchanged, except for the absence of testicular macrophages in Cl2MDP-lp-treated animals. Rats treated with NaCl or Cl2MDP-lp were injected with 100 IU of human chorionic gonadotrophin and sacrificed 2 h later. Serum testosterone concentrations increased 8.6-and 3.5-fold in NaCl and Cl2MDP-lp-treated rats, respectively, in response to acute human chorionic gonadotrophin treatment. These results point out the relevance of testicular macrophages for the regulation of the pituitary–testicular axis.
F Gaytan, Department of Cell Biology, School of Medicine, 14071 Córdoba, Spain
β-Adrenergic receptors are involved in histamine-induced secretion of proopiomelanocortin-derived peptides and prolactin in rats
Authors: Kjær Andreas , Knigge Ulrich , Matzen Steen , Warberg Jørgen 
Published: December 2008

Kjær A, Knigge U, Matzen S, Warberg J. β-Adrenergic receptors are involved in histamine-induced secretion of proopiomelanocortin-derived peptides and prolactin in rats. Eur J Endocrinol 1995;132: 223–8. ISSN 0804–4643
The neurotransmitter histamine (HA) is involved in central regulation of secretion of prolactin (PRL) and the proopiomelanocortin (POMC)-derived peptides adrenocorticotropin (ACTH), β-endorphin (β-END) and α-melanocyte-stimulating hormone (α-MSH). The effect of HA on POMC-derived peptides and PRL release is, at least in part, indirect and may involve activation of catecholaminergic systems. Therefore, we investigated the effect of β-adrenergic receptor blockade on HA or HA agonist-induced release of ACTH, β-END, α-MSH and PRL. Central administration of HA, the H1-receptor agonist 2-thiazolylethylamine (2-TEA) or the H2-receptor agonist 4-methylhistamine (4-MeHA) stimulated the secretion of ACTH, β-END, α-MSH and PRL. Pretreatment with the β-adrenergic antagonist propranolol inhibited secretion of the POMC peptides in response to HA, 2-TEA or 4-MeHA. Propranonol only inhibited the PRL response to HA or 2-TEA, but had no effect on the PRL response to 4-MeHA. Administration of the β-receptor agonist isoproterenol stimulated ACTH, β-END, α-MSH and PRL two to five-fold. This effect was totally blocked by pretreatment with propranolol. We conclude that HA-induced secretion of POMC-derived peptides from the anterior and intermediate lobe of the pituitary gland and of PRL from the anterior lobe is, at least in part, mediated via catecholamines. β-Adrenergic receptors are involved in the mediation of the POMC response to H1- as well as H2-receptor activation, whereas β-receptors are involved only in the mediation of the PRL response to H1-receptor activation.
Andreas Kjær, Department of Medical Physiology, Division of Endocrinology and Metabolism, The Panum Institute (Building 12.3), University of Copenhagen, Blegdamsvej 3c, DK-2200 Copenhagen N, Denmark
Analysis of retroorbital T cell antigen receptor variable region gene usage in patients with Graves' ophthalmopathy
Authors: Heufelder Armin E , Herterich Steffen , Ernst Gabriele , Bahn Rebecca S , Scriba Peter C 
Published: December 2008

Heufelder AE, Herterich S, Ernst G, Bahn RS, Scriba PC. Analysis of retroorbital T cell antigen receptor variable region gene usage in patients with Graves' ophthalmopathy. Eur J Endocrinol 1995; 132: 266–77. ISSN 0804–4643
To date, it has remained unclear whether orbit-infiltrating T cells in patients with Graves' ophthalmopathy (GO) represent a primary immune response in which a limited number of T cell clones driving the disease are activated against specific antigens, or whether they participate in a non-specific inflammatory process. To characterize these T cells at the molecular level, we examined the T cell antigen receptor (TcR) V gene repertoire in situ in retroorbital tissue specimens obtained from patients with early and late stages of clinically severe GO and from patients with non-GO orbital conditions. Ribonucleic acid extracted from orbital tissue and peripheral blood lymphocytes (PBL) was reverse transcribed and amplified using the polymerase chain reaction and 22 Vα and 24 Vβ genespecific oligonucleotide primers. The resulting TcR Vα and Vβ transcripts were verified by Southern hybridization analysis using TcR C region-specific, digoxigenin-labeled oligonucleotide probes. Compared with matched PBL, the retroorbital TcR Vα and Vβ gene repertoire expressed was heterogeneous, but revealed marked restriction of V gene usage in samples derived from retroorbital connective tissue and extraocular muscle of all eight patients with severe GO of short duration studied. In contrast, greater diversity of the TcR Vβ gene repertoire and loss of TcR Vα gene restriction was noted in four patients with late GO undergoing reconstructive eye muscle surgery. Unrestricted TcR V gene usage was demonstrated in orbital tissue and PBL samples obtained from control subjects. These results suggest that retroorbital TcR V gene usage is variable but markedly restricted during the earlier stages of GO. With increasing disease duration, greater diversity of the TcR V gene repertoire appears to develop, and oligoclonality of the T cell response may be lost. Selection of patients with early stages of GO will be important when further dissecting TcR usage and antigen specificity of orbit-infiltrating T lymphocytes in GO.
Armin E Heufelder, Molecular Thyroid Research Unit, Lab 280, Medizinische Klinik, Klinikum Innenstadt, Ludwig-Maximilians-Universität, Ziemssenstraße 1, 80336 München, Germany
A case of 16-ene-synthetase deficiency in male pseudohermaphroditism due to combined 17α-hydroxylase/17,20-lyase deficiency
Authors: Oei S Guid , Derksen Jan , Weusten Jos JAM , Lentjes Eef GWM , Helmerhorst Frans M 
Published: December 2008

Oei SG, Derksen J, Weusten JJAM, Lentjes EGWM, Helmerhorst FM. A case of 16-ene-synthetase deficiency in male pseudohermaphroditism due to combined 17α-hydroxylase/17,20-lyasedeficiency. Eur J Endocrinol 1995;132:281–5. ISSN 0804–4643
A 17-year-old phenotypic female with primary hypergonadotropic amenorrhea, absence of secondary sexual development, hypertension and 46 XY karyotype is presented. Hormonal analysis revealed very low levels of testosterone, dehydroepiandrosterone, androstenedione, estrogens, cortisol and high levels of ACTH, progesterone, deoxycorticosterone and corticosterone. Enzyme studies of the testicular tissue after bilateral gonadectomy showed absence of 17α-hydroxylase and 17,20-lyase activity as well as 16-ene-synthetase activity. This enzyme catalyzes the reaction from pregnenolone to 5,16-androstadien-3β-ol, a sex pheromone precursor. The other enzyme systems leading from pregnenolone to testosterone were intact. This is the first report of male pseudohermaphroditism in which the combination of 17α-hydroxylase, 17,20-lyase and 16-ene-synthetase deficiency is described, indicating that all these activities might be associated with the same protein.
FM Helmerhorst, Department of Obstetrics, Gynecology and Reproductive Medicine, University Hospital Leiden, PO Box 9600, 2300 RC Leiden, The Netherlands
Growth hormone-binding protein-related immunoreactivity in the serum of patients with acromegaly is regulated inversely by growth hormone concentration
Authors: Kratzsch Jürgen , Blum Werner F , Ventz Manfred , Selisko Thomas , Birkenmeyer Gerd , Keller Eberhard 
Published: December 2008

Kratzsch J. Blum WF, Ventz M, Selisko T, Birkenmeyer G, Keller E. Growth hormone-binding proteinrelated immunoreactivity in the serum of patients with acromegaly is regulated inversely by growth hormone concentration. Eur J Endocrinol 1994;132:306–12. ISSN 0804–4643
In this report we describe a newly developed radioimmunoassay (RIA) for the determination of the high-affinity growth hormone-binding protein (GHBP) in human blood. Using this RIA for the measurement of GHBP in serum of 29 patients with acromegaly, decreased concentrations were found compared to the normal range, depending on the activity of the disease. Growth hormonebinding protein was correlated inversely to log GH (r = −0.7, p < 0.001). A weaker relationship was shown between the GHBP activity determined in a functional assay based on charcoal separation and log GH (r = −0.51, p< 0.01). While insulin-like growth factor I (IGF-I) and IGF binding protein 3 (IGFBP-3) were correlated directly to log GH (r = 0.77 and r = 0.66, p < 0.001), an inverse and weaker relationship was evident between GHBP measured by RIA and IGF-I or IGFBP-3 (r = −0.61 and r = −0.57,p < 0.01). In contrast, no correlation could be detected between data of the functional GHBP assay and IGF-I or IGFBP-3, These results suggest, that: (1) in patients with acromegaly the GH receptor density in tissue reflected by the GHBP serum levels seems to be down-regulated, depending on the increased GH level; (2) low GHBP concentrations indicate an active disease in acromegaly and may be of diagnostic interest; (3) presuming that the GH receptor density is related to GH sensitivity, the variation of GH sensitivity is less important for IGF-I and IGFBP-3 production than the circulating GH concentration, at least in the situation of acromegaly; (4) because endogenous GH does not interfere in that assay, the RIA provides a valuable tool for the investigation of regulations between GH, GHBP and the GH receptor, especially in patients with acromegaly. The GHBP levels may be used as a sensitive parameter of GH oversecretion and tissue sensitivity to this hormone.
Jürgen Kratzsch, Inst. Clin. Chem., University of Leipzig, Paul-List-Str. 13–15, D-04103 Leipzig, Germany