bluuebunny/crossref_metadata_2025_split huggingface dataset:
Combined pyridostigmine–thyrotrophin-releasing hormone test for the evaluation of hypothalamic somatostatinergic activity in healthy normal men
Authors: Yang Inmyung , Woo Jeongtaek , Kim Sungwoon , Kim Jinwoo , Kim Youngseol , Choi Youngkil 
Published: December 2008

Yang I, Woo J, Kim S, Kim J, Kim Y, Choi Y. Combined pyridostigmine–thyrotrophin-releasing hormone test for the evaluation of hypothalamic somatostatinergic activity in healthy normal men. Eur J Endocrinol 1995;133:457–62. ISSN 0804–4643
Pyridostigmine (PST), a cholinesterase inhibitor, induces a clear growth hormone (GH) release in man by suppression of hypothalamic somatostatin (SRIH). Somatostatin suppresses thyrotrophin (TSH) release in rats and men. Earlier studies showed that the thryotrophin-releasing hormone (TRH)-induced TSH response was not altered by 60–120 mg of PST. We studied whether a larger dose (180 mg) of PST can increase the TSH response to TRH. Six healthy young men were studied with the following six tests: (Test 1) 200 μg of TRH iv; (Test 2) 180 mg of PST po; (Test 3) three different doses of PST (60, 120, 180 mg) + TRH; (Test 4) 100 μg of octreotide (SMS) iv; (Test 5) SMS + TRH; (Test 6) PST + SMS + TRH. A large dose of PST (180 mg) significantly augmented GH, TSH and prolactin responses to TRH, while smaller doses of PST (60 and 120 mg) did not significantly increase the responses of GH and TSH. While the increased TRH-induced prolactin response by PST was not suppressed by SMS, the increased responses of GH and TSH were suppressed remarkably by SMS. Most of the subjects noticed a mild to moderate abdominal pain, nausea and muscular fasciculation after the administration of a large dose of PST administration. These data suggest that suppression of hypothalamic SRIH secretion by 180 mg of PST can augment the TSH response to TRH. However, the considerable side effects should be minimized before clinical application of the combined PST–TRH test.
Inmyung Yang, Division of Endocrinology, Department of Internal Medicine, Kyunghee University School of Medicine, 1 Hoiki-dong, Dongdaemoon-ku, Seoul, 130–702, Korea
Dihydropyridine-like effects of amiodarone and desethylamiodarone on thyrotropin secretion and intracellular calcium concentration in rat pituitary
Authors: Roussel Jean-Paul , Grazzini Eric , Guipponi Michel , Astier Hélène 
Published: December 2008

Roussel J-P, Grazzini E, Guipponi M, Astier H. Dihydropyridine-like effects of amiodarone and desethylamiodarone on thyrotropin secretion and intracellular calcium concentration in rat pituitary. Eur J Endocrinol 1995;133:489–98. ISSN 0804–4643
Amiodarone (AM) and its major metabolite desethylamiodarone (DEA) are structurally similar to biologically active thyroid hormones. Amiodarone therapy is frequently associated with impairment of thyrotropic function, whose mechanisms are still controversial. Besides its effect on nuclear thyroid hormone binding, AM is able to displace dihydropyridine (DH) binding on membrane preparations from several tissues. By perifusing rat pituitary fragments and measuring thyrotropin (TSH) release we examined: the effect of AM on Ca2+-dependent and DHP-sensitive potentiation of the TSH response to thyrotropin-releasing hormone (TRH) induced by either triiodothyronine (T3, perifused for only 30 min before a TRH pulse) or by the prepro-TRH peptide 160–169 (PS4): and the effect of DEA on trh-induced TSH response in the presence or absence of the DHP nifedipine. We show that AM reverses T3 or PS4 potentiation of the TSH response to TRH; this effect is specific because AM does not modify does potentiation of that response. In contrast, DEA significantly potentiates the TSH response to TRH and the DHP nifedipine reverses that potentiation. We also tested whether Am would change the acute T3-induced increase in intracellular Ca2+ concentration by measuring intracellular Ca2+ ([Ca2+])i with fura-2 imaging on primary cultures of pituitary cells. We show that AM reverses the effect of T3 on [Ca2+]i as well as the PS4-induced increase in [Ca2+]i. In contrast, DEA increases [Ca2+]i and nifedipine reverses this effect. Our results suggest that AM and DEA display DHP-like effects on TRH-induced TSH release, behaving either as a Ca2+ channel blocker (AM) or as a Ca2+ channel agonist (DEA).
H Astier, Laboratoire de Neurobiologie Endocrinologique, URA 1197 CNRS, Departement de Biologie-Santé Université de Montpellier 2, Place E. Bataillon, 34095 Montpellier Cedex 05, France
Ascorbate depletion prevents aldosterone stimulation by sodium deficiency in the guinea pig
Authors: Redmann A , Möbius K , Hiller HH , Oelkers W , Bähr V 
Published: December 2008

Redmann A, Möbius K, Hiller HH, Oelkers W, Bähr V. Ascorbate depletion prevents aldosterone stimulation by sodium deficiency in the guinea pig. Eur J Endocrinol 1995;133:499–506. ISSN 0804–4643
The concentration of ascorbic acid (vitamin C) in the adrenal cortex is higher than in any other organ. The role of vitamin C in the adrenal cortex is unknown, but data obtained with bovine adrenocortical cells in vitro favour its role as an antioxidant that especially protects aldosterone synthesis from damaging lipid peroxides. Alternatively, vitamin C could act as part of an auxiliary electron transport system for the last step of aldosterone synthesis. The effects of vitamin C depletion on adrenocortical function cannot be studied in the human for ethical reasons, so we subjected different groups of guinea pigs to vitamin C depletion, sodium depletion and combined vitamin C and sodium depletion. Other groups of animals on normal or vitamin C-deficient diets received high-dose adrenocorticotrophin (ACTH) injections for 3 days before sacrifice. Fifteen days of a vitamin C-free diet led to very low vitamin C levels in adrenals, liver and plasma without clear signs of scurvy. At this time, plasma aldosterone and aldosterone secretion by isolated adrenal cells were stimulated significantly by sodium deficiency. Simultaneous vitamin C depletion completely abolished the rise in aldosterone in vivo and in vitro, significantly reduced the conversion of [3H]deoxycorticosterone to [3H]aldosterone and impaired renal sodium conservation. Plasma renin activity (PRA), plasma ACTH and serum potassium were not different in the sodium-depleted and sodium plus vitamin C-depleted groups. Sodium depletion did not affect cortisol. Vitamin C depletion led to a significant increase in plasma cortisol without an increase in ACTH, while in vitro secretion of cortisol was slightly decreased. These findings seem to be due to decreased hepatic cortisol metabolism. Three days of ACTH treatment led to a large increase in plasma cortisol and in vitro cortisol secretion, while plasma aldosterone and in vitro aldosterone secretion (and PRA) were greatly suppressed. This effect of ACTH was not changed by vitamin C depletion. In conclusion, our studies have demonstrated for the first time a permissive role of vitamin C in the adaptation of aldosterone secretion and of sodium excretion to sodium deficiency, which is an important physiological function of aldosterone. The molecular mechanisms by which vitamin C is involved in aldosterone synthesis await further studies.
V Bähr, Freie Universität Berlin, Klinikum Benjamin Franklin, Division of Endocrinology, Department of Medicine, Hindenburgdamm 30, D-12200 Berlin, Germany
Selective increases in adrenal steroidogenic capacity during acute respiratory disease in infants
Authors: Hanukoglu Aaron , Fried Daniel , Nakash Ishak , Hanukoglu Israel 
Published: December 2008

Hanukoglu A, Fried D, Nakash I, Hanukoglu I. Selective increases in adrenal steroidogenic capacity during acute respiratory disease in infants. Eur J Endocrinol 1995;133:552–6. ISSN 0804–4643
To examine steroidogenic responses of the different zones of the adrenal cortex to acute disease we determined the basal and adrenocorticotropin (ACTH)-stimulated levels of cortisol, dehydroepian-drosterone (DHEAS) and aldosterone in 16 infants aged 1–4 months with acute bronchiolities, Fourteen of the infants were retested after recovery. During illness the mean basal levels of cortisol and DHEAS were twice as high as the levels after recovery (370 vs 180 nmol/l and 2.7 vs 1.3 μmol/l, respectively). The mean peak ACTH-stimulated levels of cortisol and DHEAS during illness were 1.5and 2.5-fold higher, respectively, than the levels found after recovery. Although aldosterone secretion was stimulated ⩾ 3-fold by ACTH, illness was not associated with any change in aldosterone secretory capacity. The basal and stimulated levels of both cortisol and DHEAS during illness and after recovery were correlated significantly. Thus, the relative steroidogenic capacities for these two steroids were characteristic of the individual infant and showed constancy over a period of at least several weeks. While the levels of cortisol and aldosterone were not dependent on the age of the infants, both the basal and stimulated levels of DHEAS correlated strongly with age. We conclude that during acute disease the steroidogenic capacity selectively increases in the zones that secrete cortisol and DHEAS (only in infants <3 months) but not in the zona glomerulosa that secretes aldosterone. The DHEAS response may be related to its putative effects to enhance immune responses.
Aaron Hanukoglu, Department of Pediatrics, E. Wolfson Hospital, Holon 58100, Israel
Interactions between angiotensin II and norepinephrine on renin release by juxtaglomerular cells
Authors: Ichihara Atsuhiro , Suzuki Hiromichi , Murakami Marohito , Naitoh Mareo , Matsumoto Akira , Saruta Takao 
Published: December 2008

Ichihara A, Suzuki H, Murakami M, Naitoh M, Matsumoto A, Saruta T. Interactions between angiotensin II and norepinephrine on renin release by juxtaglomerular cells. Eur J Endocrinol 1995:133:569–77. ISSN 0804–4643
While the interactions between angiotensin II (Ang II) and norepinephrine (NE) on cardiovascular responses are well known, their effects on renin responses are not. We determined the renin secretion rate (RSR) and intracellular calcium level in juxtaglomerular cells harvested from Sprague-Dawley rats using a radioimmunoassay and a two-dimensional calcium analyzer. The effect of Ang II and NE was inhibitory on RSR and stimulatory on intracellular calcium. The NE-induced RSR response was amplified in the presence of Ang II (20 nmol/l), The NE-induced intracellular calcium response was also potentiated by the Ang II. There was a significant correlation (r = 0.994, p < 0.0001) between the changes in the RSR and those in intracellular calcium levels. Losartan (0.1 μmol/l), an Ang II type I receptor antagonist, blocked the Ang II threshold RSR responses and completely abolished the Ang II-related enhancements. The exclusion of calcium from the buffer reduced the maximal RSR response to NE but did not prevent the enhancement, suggesting the importance of the mobilization of intracellular calcium in the mechanism. The Ang Il-induced RSR was amplified in the presence of NE (0.2 μmol/l), The Ang II-induced intracellular calcium response was also potentiated by the NE. A significant correlation (r = 0.996, p < 0.0001) between the changes in the RSR and the changes in intracellular calcium levels was also noted. Prazosin (1 μmol/l), an α1-adrenoceptor antagonist, blocked the NE threshold RSR responses and abolished the agonist-related enhancements. The calcium-free buffer diminished this amplication with a slight decrease in the maximum RSR response to Ang II. In juxtaglomerular cells, Ang II and NE amplified each other's RSR responses via an increase in intracellular calcium levels. These responses were mediated by the activation of Ang II type I receptors and α1-adrenoceptors, respectively.
Takao Saruta, Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160, Japan
Usefulness of recombinant human prolactin for treatment of poor puerperal lactation in a rat model
Authors: Yoneda Naoto , Irahara Minoru , Saito Seiichiro , Uemura Hirokazu , Aono Toshihiro 
Published: December 2008

Yoneda N, Irahara M, Saito S, Uemura H, Aono T. Usefulness of recombinant human prolactin for treatment of poor puerperal lactation in a rat model. Eur J Endocrinol 1995;133:613–7. ISSN 0804–4643
Recombinant human prolactin (r-hPRL) was produced by a line of murine C127 cells transfected with human PRL gene. To assess the biological efficacy of r-hPRL in vivo, we studied its influence on milk secretion using a rat model in which lactation was reduced by bromocriptine treatment. Puerperal rats were injected daily for 9 days after delivery with bromocriptine or bromocriptine plus r-hPRL, and lactational performance was assessed by weighing the pups. The concentrations of rat and human PRL in rat serum were measured by specific radioimmunoassays and the mammary glands were examined on postpartum day 10. Daily injection of bromocriptine (0.1 mg/rat) significantly reduced the endogenous level of rat PRL and impaired the weight gain of the pups. Administration of r-hPRL increased the serum level of human PRL. Daily injections of r-hPRL (50 μg/rat, twice a day) restored lactational performance and significantly increased the weight of the pups. The detrimental effect of bromocriptine on the mammary glands, assessed by both weight and histological appearance, was reversed by administration of r-hPRL. These results demonstrate that r-hPRL is biologically active in vivo and replacement therapy of r-hPRL is effective in improving the lactational performance in bromocriptine-treated rats, and also that r-hPRL may be useful for the treatment of women with poor lactation.
Naoto Yoneda, Department of Obstetrics and Gynecology, School of Medicine, The University of Tokushima, 3-18-15 Kuramoto, Tokushima 770, Japan
Effect of human galanin on the response of circulating catecholamines to hypoglycemia in man
Authors: degli Uberti Ettore C , Ambrosio Maria R , Bondanelli Marta , Transforini Giorgio , Valentini Alberto , Rossi Roberta , Margutti Angelo , Campo Michela 
Published: December 2008

degli Uberti EC, Ambrosio MR, Bondanelli M, Trasforini G, Valentini A, Rossi R, Margutti A, Campo M. Effect of human galanin on the response of circulating catecholamines to hypoglycemia in man. Eur J Endocrinol 1995;133:723–8. ISSN 0804–4643
Human galanin (hGAL) is a neuropeptide with 30 amino acid residues that has been found in the peripheral and central nervous system, where it often co-exists with catecholamines. In order to clarify the possible role of hGAL in the regulation of sympathoadrenomedullary function, the effect of a 60 min infusion of hGAL (80 pmol·kg−1 · min−1) on plasma epinephrine and norepinephrine responses to insulin-induced hypoglycemia in nine healthy subjects was investigated. Human GAL administration significantly reduced both the release of basal norepinephrine and the response to insulin-induced hypoglycemia, whereas it attenuated the epinephrine response by 26%, with the hGAL-induced decrease in epinephrine release failing to achieve statistical significance. Human GAL significantly increased the heart rate in resting conditions and clearly exaggerated the heart rate response to insulin-induced hypoglycemia, whereas it had no effect on the blood pressure. We conclude that GAL receptor stimulation exerts an inhibitory effect on basal and insulin-induced hypoglycemia-stimulated release of norepinephrine. These findings provide further evidence that GAL may modulate sympathetic nerve activity in man but that it does not play an important role in the regulation of adrenal medullary function.
Ettore C degli Uberti, Chair of Endocrinology, University of Ferrara, Via Savonarola 9, I-44100 Ferrara, Italy
Familianl dysalbuminemic hyperthyroxinemia in pregnancy
Authors: Sachmechi Issac , Schussler George C 
Published: December 2008

Sachmechi I, Schussler GC. Familial dysalbuminemic hyperthyroxinemia in pregnancy. Eur J Endocrinol 1995;133:729–31. ISSN 0804–4643
A 16-year-old pregnant Puerto Rican woman who had been treated for thyrotoxicosis previously was evaluated for goiter, increased total thyroxine (T4) and triiodothyronine (T3) and free T4 estimate, despite a normal thyroid-stimulating hormone (TSH) concentration. These findings are consistent with a TSH-producing pituitary adenoma or the syndrome of generalized thyroid hormone resistance. However, sera from the patient, her mother and subsequently her newborn daughter demonstrated the increased albumin binding of T4 but not T3 that is characteristic of familial dysalbuminemic hyperthyroxinemia (FDH). The free T4 estimate had been elevated artefactually by the increased affinity of FDH albumin for the analog in a one-step assay. The T3 and T4 concentrations were increased by pregnancy and T4 was increased further by FDH. This first report of FDH recognized during pregnancy emphasizes that the effects of pregnancy on thyroid hormone and TSH concentrations complicate the diagnosis of FDH. It is particularly important to distinguish this benign condition from thyrotoxicosis during pregnancy, because inappropriate treatment may affect fetal development.
Issac Sachmechi, Dept. of Medicine, Queens Hospital Center, 82-68 164th Street, Queens, New York, USA
Melatonin affects proopiomelanocortin gene expression in the immune organs of the rat
Authors: Wajs Ewa , Kutoh Eiji , Gupta Derek 
Published: December 2008

Wajs E, Kutoh E, Gupta D. Melatonin affects proopiomelanocortin gene expression in the immune organs of the rat. Eur J Endocrinol 1995;133:754–60. ISSN 0804–4643
The induction of opioid peptides derived from cells of the immune system is postulated to be the main mechanism involved in the immunomodulatory role of melatonin. In this study, it has been demonstrated for the first time that melatonin can act on the level of proopiomelanocortin (POMC) gene expression. The effect of the pineal hormone, administered in late-afternoon subcutaneous injections, was studied in the immune organs of adult male Wistar rats by means of a highly sensitive reverse transcription-polymerase chain reaction method (RT-PCR), followed by polyacrylamide gel electrophoresis and densitometric analysis of the bands. It was demonstrated that melatonin stimulates the expression of the 3rd exon of the POMC gene in the lymph nodes and in bone marrow. No significant effects of the pineal hormone were observed in the spleen and thymus. The study establishes that the formation of short POMC transcripts in the bone marrow and lymph nodes may be upregulated by melatonin. Moreover, the pineal hormone exerts its effect without antigenic stimulation.
Ewa Wajs, Section Pediatric Endocrinology, Children's Hospital, The University of Tübingen, Rümelinstr. 23, 72070 Tübingen, Germany
Characterization of adhesion receptors on cultured microvascular endothelial cells derived from the retroorbital connective tissue of patients with Graves' ophthalmopathy
Authors: Heufelder Armin E , Scriba Peter C 
Published: December 2008

Heufelder AE, Scriba PC. Characterization of adhesion receptors on cultured microvascular endothelial cells derived from the retroorbital connective tissue of patients with Graves' ophthalmopathy. Eur J Endocrinol 1996:134:51–60
T lymphocytes have been demonstrated recently to play an important role in the pathogenesis and propagation of Graves' ophthalmopathy (GO). Recruitment of T cells to the retroorbital tissue in GO involves the activation of certain adhesion molecules both in the vascular endothelium and in the extravascular connective tissue within the retroorbital space. To characterize the interactions between orbital endothelial cells (OECs) and circulating T cells in vitro, we designed a two-step immunopurification procedure with bead-immobilized Ulex europaeus I lectin and anti-human endothelial cell antigen (CD3I) monoclonal antibody for rapid and reproducible isolation of highly pure microvascular endothelial cell populations from small quantities of retroorbital connective tissue. Endothelial origin of the resulting cell populations was confirmed by positive immunoreactivity for von Willebrand factor. CD 3 I and thrombomodulin. Under baseline conditions, GO-OECs, but not normal OECs, expressed intercellular adhesion molecule 1 (ICAM-1) and CD44 immunoreactivity but no immunoreactivity for endothelial leukocyte adhesion molecule I (ELAM-1) and vascular cell adhesion molecule I (VCAM-1) was detected. Exposure of GO-OEC and normal OEC monolayers to interferon γ, interleukin 1 α and tumor necrosis factor α resulted in marked up-regulation of immunoreactivity for ICAM-1 and in induction of ELAM-1 and VCAM-1. Blocking experiments using monoclonal antibodies directed against various adhesion molecules demonstrated that interactions between matched activated T lymphocytes and OECs were mediated by integrin-dependent ICAM-1/leukocyte function-associated antigen 1 (LFA-1): VCAM-1/very late antigen 4 (VLA-4)) and integrin-independent (CD44) pathways, and revealed marked differences when comparing GO-OECs and normal OECs. In conclusion, the availability of OECs from affected retroorbital tissue of patients with GO provides a valuable tool for studying further the mechanisms responsible for orbit-specific lymphocyte recruitment in GO.
Armin E Heufelder, Molecular Thyroid Research Unit, Medizinische Klinik, Klinikum Innenstadt, Ziemssenstrasse 1, 80336 München, Germany
Effects of castration on luteinizing hormone secretion and response to gonadotrophin-releasing hormone in sheep infected with Trypanosoma congolense
Authors: Mutayoba BM , Eckersall PD , Jeffcoate IA , Harvey MJA , Cestnik V , Holmes PH 
Published: December 2008

Mutayoba BM, Eckersall PD, Jeffcoate IA, Harvey MJA, Cestnik V. Holmes, PH. Effects of castration on luteinizing hormone secretion and response to gonadotrophin-releasing hormone in sheep infected with Trypanosoma congolense, Eur J Endocrinol 1996:134:115–22. ISSN 0804–4643
The effects of trypanosomiasis on the endocrine function of the hypothalamo-pituitary-gonadal axis were investigated before and after castration of Scottish Blackface rams infected with Trypanosoma congolense and uninfected controls. Blood samples were collected at 15-min intervals for 6 h before and at 10,20,40, 60, 80, 100 and 120 min after injection of synthetic gonadotrophin-releasing hormone (GnRH, 20 μg iv) 2 days before infection and 26 and 54 days after infection, with castration being performed 28 days after infection. Mean luteinizing hormone (LH) pulse amplitude was higher (3.3 ± 0.2 vs 2.6 ± 0.3 ng/ml) and mean plasma testosterone concentration was lower (4.1 ± 0.6 vs 7.6 ±1.2 nmol/l) in infected vs control rams 26 days after infection (p < 0.05). Mean plasma LH concentration and pulse amplitude increased in both groups after castration but both were significantly lower in infected compared to control rams (6.6 ±1.5 and 13.0 ± 2.2 ng/ml, p < 0.01; 7.7 ±0.9 and 11.6 ± 0.9 ng/ml, p < 0.001). respectively. However, LH responses to exogenous GnRH were similar in infected and control rams at each stage of the experiment, suggesting that the smaller increase in plasma LH after castration in infected rams was not caused by reduced responsiveness of the pituitary to GnRH but by alterations in GnRH secretion by the hypothalamus or its transport to the adenohypophysis. These results also demonstrate that impairment of testosterone secretion within 4 weeks of T. congolense infection in sheep may be due to testicular rather than pituitary effects.
IA Jeffcoate, Department of Veterinary Physiology. University of Glasgow Veterinary School, Bearsden, Glasgow G61 1QH. UK