bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of hypothyroidism on ovarian follicular development, granulosa cell proliferation and peripheral hormone levels in the prepubertal rat
Authors: Dijkstra Grietje , de Rooij Dirk G , de Jong Frank H , van den Hurk Robert 
Published: December 2008

Dijkstra G, de Rooij DG, de Jong FH, van den Hurk R. Effect of hypothyroidism on ovarian follicular development, granulosa cell proliferation and peripheral hormone levels in the prepubertal rat. Eur J Endocrinol 1996;134:649–54. ISSN 0804–4643
The aim of this study was to examine the effects of prepubertal hypothyroidism on ovarian development in rats. Therefore, from birth up to day 40 postpartum, rats were given 6-propyl-2-thiouracil (PTU) via the drinking water of mothers and pups. At ages ranging from 12 to 40 days, ovarian weights were measured and serum was collected to estimate thyrotrophin (TSH), folliclestimulating hormone (FSH) and inhibin levels. Two hours before sacrifice the animals received an injection of bromodeoxyuridine (BrdU) to estimate the proliferative activity of the follicular granulosa cells. Ovaries were fixed in Carnoy's fluid and follicle counts were performed on sections stained with anti-BrdU and with haematoxylin and eosin. The PTU treatment resulted in increased serum TSH levels, indicative of hypothyroidism, and markedly lower body and ovarian weights, whereas serum FSH and inhibin levels were hardly affected. At day 40, ovaries of PTU-treated animals contained relatively more secondary and less antral follicles, smaller non-atretic antral follicles and more atretic follicles when compared with untreated rats, while corpora lutea were absent. It is concluded that this disturbed folliculogenesis is due to inadequate thyroid hormone supply, which hampers the differentiation and not the proliferation of granulosa cells because diameters of antral follicles were significantly smaller whereas the BrdU-labelling index had not changed.
Robert van den Hurk, Department of Functional Morphology, Faculty of Veterinary Medicine, PO Box 80.157, 3508 TD Utrecht, The Netherlands
Differential responses of femoral and vertebral bones to long-term excessive l-thyroxine administration in adult rats
Authors: Suwanwalaikorn Sompongse , Ongphiphadhanakul Boonsong , Braverman Lewis E , Baran Daniel T 
Published: December 2008

Suwanwalaikorn S, Ongphiphadhanakul B, Braverman LE, Baran DT. Differential responses of femoral and vertebral bones to long-term excessive l-thyroxine administration in adult rats. Eur J Endocrinol 1996;134:655–9. ISSN 0804–4643
Recent studies suggest that thyroid-stimulating hormone suppressive doses of thyroid hormone decrease bone mass in humans and growing rats. To determine the long-term effects of excessive l-thyroxine administration on the femur and vertebrae in an adult rat model, 20 male Sprague-Dawley rats (20 weeks old) were randomized into two groups. Group 1 received l-thyroxine (20 μg/100 g body weight ip daily), and group 2 received normal saline ip daily for 20 weeks. Femoral and lumbar vertebral bone mineral density measurements were performed at 0, 6, 15, 18 and 20 weeks of treatment. After 20 weeks of treatment, total RNA was isolated from both femoral and lumbar bones. Northern hybridization was performed with 32P-labeled DNA probes for osteocalcin, osteopontin, alkaline phosphatase and tartrate-resistant acid phosphatase. Significant decreases in bone mineral density in the femur of l-thyroxine-treated rats were observed after 15 weeks (p < 0.03). Lumbar bone mineral density was not affected. Both osteoblast (osteocalcin, osteopontin, alkaline phosphatase) and osteoclast (tartrate-resistant acid phosphatase) gene expression markers were increased significantly in the femoral bone (p < 0.001), but not in the lumbar vertebrae of the l-thyroxine-treated rats. We conclude that long-term administration of excessive doses of l-thyroxine to the adult rat preferentially affects femoral but not vertebral bone. This is manifested by decreased bone mineral density as well as increased gene expression markers for osteoblast and osteoclast activity in the femur.
Daniel T Baran, Department of Orthopedics, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA
Graves' disease in children and adolescents. Late results of surgical treatment
Authors: Rudberg Claes , Johansson Henry , Åkerström Göran , Tuvemo Torsten , Anders Karlsson F 
Published: December 2008

Rudberg C, Johansson H, Å&#x212B; G, Tuvemo T, Karlsson FA. Graves' disease in children and adolescents. Late results of surgical treatment. Eur J Endocrinol 1996;134:710–5. ISSN0804–4643
All children and adolescents with Graves' disease in the county of Uppsala (catchment area population 250000) treated between 1970 and 1994 were evaluated in a retrospective study. The material comprised 31 patients with a mean age of 11 years (range 4–16), 29 (94%) of whom were girls, and four (13%) of the patients had Down's syndrome. Treatment was primarily conservative and surgery was considered if prolonged medical treatment failed. Lasting remission after antithyroid drug therapy (median 6.5 years; range 4.5–8 years) was noted in 6/31 patients (19%), three (10%) of whom subsequently developed hypothyroidism. Twenty-four of the remaining patients (77%) ultimately underwent subtotal (N=20) or total thyroidectomy (N=4) after experiencing one or more episodes of recurrent hyperthyroidism during medical treatment (median 6 years; range 0.5–11 years). After surgery one patient developed permanent hypocalcemia requiring low-dose vitamin D supplementation. During a postoperative follow-up period of 12.2 years (median: range 1–17 years), there were two cases of recurrent thyrotoxicosis, 1 and 10 years after surgery. The results underline that gender and Down's syndrome are risk factors of juvenile Graves' disease and that the disorder often is difficult to control by long-term medical therapy. In such cases thyroid surgery offers a safe and prompt reversal of the thyrotoxicosis. A proportion of the patients may ultimately develop hypothyroidism, substantiating a need for long-term follow-up of persons afflicted with Graves' disease early in life.
F Anders Karlsson, Department of Medicine, University Hospital, S-751 85 Uppsala. Sweden
Characteristics of gsp-positive growth hormone-secreting pituitary tumors in Korean acromegalic patients
Authors: Yang Inmyung , Park Seungjoon , Ryu Meesook , Woo Jeongtaek , Kim Sungwoon , Kim Jinwoo , Kim Youngseol , Choi Youngkil 
Published: December 2008

Yang I, Park S, Ryu M, Woo J, Kim S, Kim J, Kim Y, Choi Y. Characteristics of gsp-positive growth hormone-secreting pituitary tumors in Korean acromegalic patients. Eur J Endocrinol 1996;134: 720–6. ISSN 0804–4643
A subset of human growth hormone (GH)-secreting pituitary tumors contains the gsp oncogene that encodes an activation mutation of the α-subunit of the stimulatory GTP-binding protein (Gsα). This study was undertaken to investigate the frequency of the gsp oncogene in GH-secreting pituitary tumors in Korean acromegalic patients and to elucidate the clinical characteristics of these patients to endocrine testing. Direct polymerase chain reaction sequencing revealed the gsp oncogene mutation in 9 out of 21 tumors (43%) at amino acid 201 of the Gsα protein. A single nucleotide mutation in the tumors carrying the gsp oncogene was observed, which replaced an arginine (CGT) in the normal protein with cysteine (TGT) in eight tumors and serine (AGT) in one tumor. The patients with the gsp oncogene mutation (group 1) were older (54 ± 10 vs 41 ±11 years, p = 0.0085) than those without the mutation (group 2). Sex, tumor size and grade, basal GH and prolactin levels, the GH response to oral glucose loading, the GH fluctuation and the paradoxical response to thyrotropin-releasing hormone or gonadotropin-releasing hormone did not differ between the groups. The gsp oncogene was found mostly in somatotroph adenomas. The octreotide-induced GH suppression was significantly higher in group 1 than in group 2 (95 ± 5% vs 81 ± 17%, p = 0.0335). The GH response to bromocriptine did not differ between the groups. These results suggest that the Gsα mutations of GH-secreting tumor are observed in Korean acromegalic patients with similar frequency to those of western countries. The patients with gsp oncogene are likely to be older than those without the oncogene, and show excellent response of GH suppression to octreotide.
Inmyung Yang, Division of Endocrinology, Department of Internal Medicine, Kyunghee University School of Medicine, 1 Hoiki-dong, Dongdaemoon-ku, Seoul 130-702, Korea
Pituitary insufficiency and regression of acromegaly caused by pituitary apoplexy following cerebral angiography
Authors: Louwerens Marloes , de Herder Wouter W , Postema Pieter TE , Tanghe Hervé LJ , Lamberts Steven WJ 
Published: December 2008

Louwerens M, de Herder WW, Postema PTE, Tanghe HLJ, Lamberts SWJ. Pituitary insufficiency and regression of acromegaly caused by pituitary apoplexy following cerebral angiography. Eur J Endocrinol 1996;134:737–40. ISSN 0804–4643
Pituitary apoplexy as a complication of cerebral angiography has been described in only a few case reports. Some studies have reported the clinical resolution of active acromegaly after pituitary apoplexy. We present a patient with active acromegaly due to a growth hormone (GH)-secreting pituitary macroadenoma, who developed anterior and posterior pituitary insufficiency following cerebral angiography. Furthermore, a significant reduction in tumour size was accompanied by normalization of mean 24 h in GH insulin-like growth factor I (IGF-I) and IGF binding protein 3 levels.
WW de Herder, Department of Internal Medicine III and Clinical Endocrinology, University Hospital Rotterdam, Dr Molewaterplein 40, 3015 GD Rotterdam, The Netherlands
Permissive role of α-tocopherol in the stimulation of aldosterone by sodium depletion in the guinea pig
Authors: Möbius K , Redmann A , Hiller HH , Oelkers W , Bähr V 
Published: December 2008

Möbius K, Redmann A, Hiller HH, Oelkers W, Bähr V. Permissive role of α-tocopherol in the stimulation of aldosterone by sodium depletion in the guinea pig. Eur J Endocrinol 1996;134:758–63. ISSN 0804–4643
To investigate the role of vitamin E in aldosterone synthesis, in vivo and in vitro studies were done in α-tocopherol-depleted guinea pigs. Seventy-one days of low vitamin E intake (< 5 mg/kg feed) reduced the concentration of α-tocopherol in serum, liver and adrenals to low levels with no signs of hypovitaminosis. Aldosterone secretion was stimulated by 15 days on a low sodium diet (200 mg/kg feed) in controls and vitamin E-depleted animals. Sodium depletion in controls stimulated plasma aldosterone by 335%. Vitamin E depletion reduced the stimulation of plasma aldosterone to only 112% (p < 0.05). In vitro aldosterone secretion by adrenal cells from sodium-depleted animals was 252% higher than secretion by cells from controls. This enhancement of in vitro aldosterone secretion following in vivo sodium depletion was abolished completely by combined in vivo vitamin E and sodium depletion (p < 0.05). No significant differences between groups were found for plasma renin activity, adrenocorticotrophin and serum potassium, suggesting that intra-adrenal mechanisms like damage by enhanced lipid peroxidation in α-tocopherol-depleted animals rather than changes in humoral aldosterone-regulating factors are the cause of the attenuated aldosterone response to sodium depletion.
Volker Bähr, Abteilung Endokrinologie, Medizinische Klinik, Klinikum Benjamin Franklin, Freie Universität Berlin, Hindenburgdamm 30, D-12000 Berlin, Germany
Coordinate expression of insulin-like growth factor II (IGF-II) and IGF-II/mannose-6-phosphate receptor mRNA and stable expression of IGF-I receptor mRNA during differentiation of human colon carcinoma cells (Caco-2)
Authors: Hoeflich Andreas , Yang Yi , Rascher Wolfgang , Blum Werner F , Huber Stefan , Koepf Gabriele , Kolb Helmut J , Kiess Wieland 
Published: December 2008

Hoeflich A, Yang Y, Rascher W, Blum WF, Huber S, Koepf G, Kolb HJ, Kiess W. Coordinate expression of insulin-like growth factor II (IGF-II) and IGF-II/mannose-6-phosphate receptor mRNA and stable expression of IGF-I receptor mRNA during differentiation of human colon carcinoma cells (Caco-2). Eur J Endocrinol 1996;135:49–59. ISSN 0804–4643
Insulin-like growth factor II (IGF-II) has been implicated in the differentiation of skeletal muscle cells. In this study the putative role of IGF-II in epithelial cell differentiation was investigated. The expression of IGF-II, IGF-1 receptor and IGF-II/mannose-6-phosphate receptor (IGF-II/M6P receptor) mRNA during spontaneous differentiation of the colon carcinoma cell line Caco-2 was measured. In addition, differentiation of Caco-2 cells during the cell culture period (days 1–21 in culture) was studied in parallel using morphological (light and scanning electron microscopy) and biochemical markers of growth (DNA, RNA and protein content, and β-actin mRNA and glyceraldehyde phosphate dehydrogenase mRNA expression) and differentiation (alkaline phosphatase activity, carcinoembryonic antigen content). A putative correlation between the markers of growth and differentiation and IGF gene expression was studied using linear regression analysis. Expression of IGF-II mRNA and IGF-II/M6P receptor mRNA correlated significantly with the progress of differentiation, while the IGF-I receptor was stably expressed throughout the culture period and exhibited a crucial role for the survival of Caco-2 cells, as shown by blocking experiments employing the monoclonal anti-IGF-I receptor antibody alpha-IR3. We hypothesize that: IGF-II mRNA and IGF-II/M6P receptor mRNA are expressed in a coordinate fashion during the differentiation of Caco-2 cells; coordinate expression of IGF-II and of IGF-II/M6P receptor mRNA might point to a role for IGF-II as a growth stimulant and for the IGF-II/M6P receptor for a regulator of IGF-II bioavailability in differentiating cells; alternatively, high IGF-II/M6P receptor mRNA and protein expression in differentiated cells but low IGF-II binding to the IGF-II/M6P receptor point to an important intracellular role of this receptor type in differentiated colon epithelial cells; the IGF-I receptor mRNA is stably expressed during the differentiation process of Caco-2 cells; the IGF-I receptor protein seems to be a prerequisite for the survival of Caco-2 cells.
W Kiess, Children's Hospital, Justus Liebig University, Feulgenstr. 12, D-35385 Giessen, Germany
Fracture rate, pre- and postmenopausal bone mass and early and late postmenopausal bone loss are not associated with vitamin D receptor genotype in a high-endemic area of osteoporosis
Authors: Berg Jens P , Falch Jan A , Haug Egil 
Published: December 2008

Berg JP, Falch JA, Haug E, Fracture rate, pre- and postmenopausal bone mass and early and late postmenopausal bone loss are not associated with vitamin D receptor genotype in a high-endemic area of osteoporosis. Eur J Endocrinol 1996;135:96–100. ISSN 0804–4643
To investigate a possible association between vitamin D receptor genotype and development of postmenopausal osteoporosis, a longitudinal study from 1977 to 1995 was carried out on women living in Oslo, Norway. One hundred and eighteen premenopausal women born in 1930 were included in a study of pre- and postmenopausal bone loss in 1977. In 1995, blood samples for vitamin D receptor genotyping were available in 72, 42 and 49 of the women eligible for the determination of premenopausal bone mineral content, early postmenopausal appendicular bone loss and late postmenopausal bone mineral content, bone loss and fractures, respectively. Bone mineral density was measured in the distal and proximal right forearm annually from 1977 to 1987, and in the lumbar spine, proximal femur, right forearm and total body, including ultrasound measurements of the right calcaneus, in 1993 and 1995. Non-spinal fractures were also recorded. The results were compared to the individual vitamin D receptor genotype and it was found that vitamin D receptor genotype was neither associated with non-spinal fractures, pre- and postmenopausal bone mass nor with early and late postmenopausal bone loss within the age of 65 years. In conclusion, premenopausal bone mass, postmenopausal bone loss and the subsequent risk of osteoporosis and fractures were not predicted by vitamin D receptor genotype in a high-endemic area of osteoporosis.
Jens P Berg, Hormone Laboratory, Aker University Hospital, Trondheimsveien 235, N-0514 Oslo, Norway
Effects of insulin-like growth factor I on growth, epithelial barrier and iodide transport in polarized pig thyrocyte monolayers
Authors: Ericson Lars E , Nilsson Mikael 
Published: December 2008

Ericson LE, Nilsson M. Effects of insulin-like growth factor I on growth, epithelial barrier and iodide transport in polarized pig thyrocyte monolayers. Eur J Endocrinol 1996;135:118–27. ISSN 0804–4643
The effects of insulin-like growth factor I (IGF-I) on mitogenesis, epithelial barrier function and transepithelial iodide transport were studied in confluent, polarized monolayers of pig thyrocytes cultured on filter in Transwell bicameral chambers. The growth rate in controls cultured in 1% fetal calf serum was low. Insulin-like growth factor I stimulated dose-dependently the incorporation of [3H]thymidine, maximally at 100 ng/ml, which corresponded to an increase of DNA content by 60% after 6 days. Thyrotropin (1 mU/ml) alone did not stimulate cell multiplication but inhibited partially the stimulatory effect of IGF-I. Insulin-like growth factor I(100 ng/ml) increased within 10 min the transepithelial potential difference, which remained elevated for several days, but did not significantly change the transepithelial resistance. When added together, IGF-I reinforced the effects of TSH on potential difference (increase) and resistance (decrease). A preserved epithelial barrier in IGF-I-treated cultures was confirmed by observing a normal immunolocalization of the tight junction protein ZO-1 and an unchanged ultrastructure of the junctional complex. Insulin-like growth factor I increased the transepithelial flux of 125I− in the basal-to-apical, but not in the opposite, direction. Stimulation of iodide transport by IGF-I was modest after 2 days and pronounced after 6 days. In comparison, TSH-stimulated iodide transport was higher after 2 days but lower after 6 days. Both TSH and IGF-I were strongly synergistic, after 6 days amounting to a 90-fold increase over the control basoapical 125I− transfer. The simultaneous accumulation of 125I− in the cell layer was increased two- to fourfold by IGF-I and/or TSH. In conclusion, IGF-I is able to induce growth in preformed monolayers of pig thyrocytes cultured on permeable filter. During these conditions, the mitogenic effect of IGF-I is partially inhibited by TSH, which has no growth-promoting action on its own. The transepithelial transport of iodide and bulk electrolytes is altered by IGF-I without affecting the epithelial barrier function. Specifically, IGF-I up-regulates the activity of the basolateral iodide pump and increases the iodide permeability of the apical plasma membrane. The action of IGF-I on iodide transport is independent of, although synergistic with, that of TSH. The findings support the notion that IGF-I may be an important regulator of thyroid growth and differentiated functions.
Lars E Ericson, Institute of Anatomy and Cell Biology, Göteborg University, Medicinaregatan 3, S-413 90 Göteborg, Sweden
Melatonin receptors in the chicken kidney are up-regulated by pinealectomy and linked to adenylate cyclase
Authors: Song Y , Pang CS , Ayre EA , Brown GM , Pang SF 
Published: December 2008

Song Y, Pang CS, Ayre EA, Brown GM, Pang SF. Melatonin receptors in the chicken kidney are upregulated by pinealectomy and linked to adenylate cyclase. Eur J Endocrinol 1996;135:128–33. ISSN 0804–4643
The effect of pinealectomy on the characteristics of melatonin receptors in the chicken kidney was studied. One-day-old chicks were operated and kept under a 12 h/12 h light/dark photoperiod. Six weeks after operation, the animals were sacrificed at mid-light and mid-dark. Serum melatonin was determined by radioimmunoassay and kidney melatonin receptors were studied by radioreceptor assay using the melatonin agonist 2-[125I]iodomelatonin as the radioligand. Pinealectomy significantly reduced the mid-dark serum melatonin level and abolished the diurnal rhythm of 2-[125I]iodomelatonin binding in the kidney. The density of 2-[125I]Iodomelatonin binding sites in the kidney at mid-dark was increased significantly to a value comparable to the mid-light density after pineal ablation. Our results suggest that melatonin receptors in the chicken kidney are directly regulated by melatonin in the circulation. The coupling of kidney melatonin receptors to adenylate cyclase was investigated. The basal and forskolin-stimulated cAMP production in chicken kidney explants was studied following melatonin or melatonin plus pertussis toxin treatment. Levels of cAMP in chicken kidney explants were extracted and determined by radioimmunoassay. Melatonin had no effect on basal cAMP levels. However, melatonin significantly inhibited the forskolin-stimulated cAMP accumulation at a concentration of 10 pmol/l. Inhibitory effects of melatonin on the forskolin-stimulated cAMP increase in the chicken kidney were totally blocked by preincubating the kidney tissue with 1.0 μg/ml pertussis toxin. Our results suggest that kidney melatonin receptors may modulate the adenylate cyclase leading to biological responses in the renal system.
SF Pang, Department of Physiology, Faculty of Medicine, University of Hong Kong, Hong Kong
Neuroendocrine regulation of pituitary–adrenal function during fetal life
Authors: Brooks AN , Hagan DM , Howe DC 
Published: December 2008

Brooks AN, Hagan DM, Howe DC. Neuroendocrine regulation of pituitary–adrenal function during fetal life. Eur J Endocrinol 1996;135:153–65. ISSN 0804–4643
During late gestation there is a rise in the concentration of corticosteroids in the fetal circulation that is essential for the coordinated maturation of many fetal organ systems and is a key component in the endocrine pathway leading to the onset of birth. Fetal plasma concentrations of adrenocorticotrophin (ACTH) increase during late, gestation and this rise precedes the increase in plasma corticosteroids. Paradoxically, ACTH and cortisol concentrations increase concomitantly even though cortisol would normally be expected to exert negative feedback effects to inhibit pituitary ACTH secretion. Elucidating the neuroendocrine signals that cause the increase in fetal ACTH, despite the elevated concentrations of cortisol at this time, will therefore provide vital clues as to the trigger for fetal organ maturation and birth. This article describes the normal ontogeny of the hypothalamo–pituitary–adrenal axis, discusses the neuroendocrine signals that trigger the increase in fetal ACTH secretion and provides potential explanations for the concomitant rise in ACTH and cortisol.
AN Brooks, MRC Reproductive Biology Unit, 37 Chalmers Street, Edinburgh, EH3 9EW, Scotland, UK