bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation of mouse placental lactogen secretion by factors secreted from the pituitary in vitro
Authors: Yamaguchi Masaaki , Miyake Akira 
Published: December 2008

Yamaguchi M. Miyake A. Regulation of mouse placental lactogen secretion by factors secreted from the pituitary in vitro. Eur J Endocrinol 1996;134:123–7. ISSN 0804–4643
The effect of factors secreted from the pituitary on mouse placental lactogen I (mPL-I) and mPL-II secretion in vitro was examined. Co-culture of mouse placental cells from day 7 of pregnancy with the pituitary cells of the mother significantly stimulated mPL-I secretion but did not regulate mPL-II secretion. The effect on mPL-I secretion was dependent on the number of pituitary cells. The conditioned medium of pituitary cells also significantly stimulated mPL-I secretion but did not regulate mPL-II secretion. The stimulatory effect of mPL-I secretion was dependent on the volume of the conditioned medium. The number of cells containing mPL-I assessed by immunocytochemistry was increased by the co-culture in a cell number-dependent manner. Northern blot analysis for mPL-I indicated that treatment of placental cells with the pituitary-conditioned medium results in an increase of mPL-I gene expression. These findings suggest that factors secreted from the pituitary directly regulate mPL-I secretion, but not mPL-II secretion, before midpregnancy in vivo.
Masaaki Yamaguchi, Department of Obstetrics and Gynecology. Osaka University Medical School, 2-2 Yamadaoka, Suita. Osaka 565, Japan
Restoration of human chorionic gonadotropin response in human myometrial smooth muscle cells by treatment with follicle-stimulating hormone (FSH): evidence for the presence of FSH receptors in human myometrium
Authors: Kornyei JL , Li X , Lei ZM , Rao ChV 
Published: December 2008

Kornyei JL, Li X, Lei ZM, Rao ChV. Restoration of human chorionic gondadotropin response in human myometrial smooth muscle cells by treatment with follicle-stimulating hormone (FSH): evidence for the presence of FSH receptors in human myometrium. Eur J Endocrinol 1996;134:225–31. ISSN 0804–4643
Human myometrial smooth muscle cells contain receptors for human chorionic gonadotropin (hCG)/ luteinizing hormone (LH). Exogenous hCG and LH can cause a modest hyperplasia in myometrial smooth muscle cells in culture. This response is lost after about the third subculture of the cells. The present study investigated whether the loss of hCG response could be restored by co-culturing with human follicle stimulating hormone (FSH). The results showed that co-culturing with FSH can indeed restore a modest mitogenic response of hCG. However, FSH alone was not mitogenic. The FSH restoration of hCG response can be blocked by antibodies to FSH or hCG but not by non-specific rabbit IgG. The FSH treatment resulted in an increase of steady state levels of hCG/LH receptor mRNA and protein in myometrial smooth muscle cells. Since the FSH actions could be receptor mediated, we investigated the presence of FSH receptor mRNA transcripts and protein in freshly dispersed myometrial smooth muscle cells. Northern blotting demonstrated that myometrial smooth muscle cells, just as rat ovary, a classical target of FSH action, contain multiple FSH receptor mRNA transcripts. Western immunoblotting demonstrated that myometrial smooth muscle cells also contain a 60 kDa FSH receptor protein just as rat ovary and human granulosa cells used as positive control tissues. The immunocytochemistry also demonstrated that myometrial smooth muscle cells, as rat ovary and human granulosa cells, contain FSH receptor immunostaining. In summary, it is novel that FSH could restore the mitogenic response of hCG in human myometrial smooth muscle cells and these cells contain FSH receptors. These findings may have functional implications for direct regulation of human myometrium not only by hCG/LH but also by FSH.
ChV Rao, Department of Obstetrics and Gynecology, 438 MDR Building, University of Louisville, School of Medicine, Louisville, Kentucky 40292, USA
Human kidney 11β-hydroxysteroid dehydrogenase: regulation by adrenocorticotropin?
Authors: Diederich S , Quinkler M , Miller K , Heilmann P , Schöneshöfer M , Oelkers W 
Published: December 2008

Diederich S, Quinkler M, Miller K, Heilmann P, Schöneshöfer M, Oelkers W. Human kidney 11βhydroxysteroid dehydrogenase: regulation by adrenocorticotropin? Eur J Endocrinol 1996;134:301–7. ISSN 0804–4643
In ectopic adrenocorticotropin (ACTH) syndrome (EAS) with higher ACTH levels than in pituitary Cushing's syndrome and during ACTH infusion, the ratio of cortisol to cortisone in plasma and urine is increased, suggesting inhibition of renal 11β-hydroxysteroid dehydrogenase (11β-HSD) by ACTH or by ACTH-dependent steroids. Measuring the conversion of cortisol to cortisone by human kidney slices under different conditions, we tested the possibility of 11β-HSD regulation by ACTH and corticosteroids. Slices prepared from unaffected parts of kidneys removed because of renal cell carcinoma were incubated with unlabeled or labeled cortisol, and cortisol and cortisone were quantitated after HPLC separation by UV or radioactive detection. The 11β-HSD activity was not influenced by incubation with increasing concentrations (10−12–10−9 mol/l) of ACTH (1–24 or 1–39) for 1 h. Among 12 ACTH-dependent steroids tested (10−9–10−6 mol/l), only corticosterone (IC50 = 2 × 10−7 mol/l), 18-OH-corticosterone and 11βOH-androstenedione showed a significant dose-dependent inhibition of 11β-HSD activity. The percentage conversion rate of cortisol to cortisone was concentration dependent over the whole range of cortisol concentrations tested (10−8–10−5 mol/l). A direct inhibitory effect of ACTH on 11β-HSD is, therefore, unlikely. The only steroids inhibiting the conversion of cortisol to cortisone are natural substrates for 11β-HSD Kinetic studies show a saturation of the enzyme at high cortisol concentrations. Thus, the reduced percentage renal cortisol inactivation in EAS seems to be due mainly to overload of the enzyme with endogenous substrates (cortisol, corticosterone and others) rather than to direct inhibition of 11β-HSD by ACTH or ACTHdependent steroids, not being substrates of 11β-HSD.
S Diederich, Department of Endocrinology, Klinikum Benjamin Franklin, Freie Universität Berlin, Hindenburgdamm 30, 12200 Berlin, Germany
Obvious mRNA and protein expression but absence of mutations of the RET proto-oncogene in parathyroid tumors
Authors: Kimura Takehiko , Yoshimoto Katsuhiko , Tanaka Chisato , Ohkura Toshihiro , Iwahana Hiroyuki , Miyauchi Akira , Sano Toshiaki , Itakura Mitsuo 
Published: December 2008

Kimura T, Yoshimoto K, Tanaka C, Ohkura T, Iwahana H, Miyauchi A, Sano T. Itakura M. Obvious mRNA and protein expression but absence of mutations of the RET proto-oncogene in parathyroid tumors. Eur J Endocrinol 1996;134:314–9. ISSN 0804–4643
The study on the expression of the RET proto-oncogene in parathyroid tumors disclosed obvious mRNA expression by the reverse transcription (RT)-polymerase chain reaction (PCR) method and protein expression by Western blotting. To find out whether mutations in the cysteine-rich regions or tyrosine kinase domain of the RET proto-oncogene are etiological for parathyroid tumorigenesis, sporadic parathyroid adenomas and carcinomas, parathyroid tumors from multiple endocrine neoplasia 1. familial isolated hyperparathyroidism or hereditary hyperparathyroidism-jaw tumor syndrome were screened by PCR-single strand conformation polymorphism and PCR restriction fragment length polymorphism. Missense mutations in the cysteine-rich region, or codons 768 or 918 in the tyrosine kinase domain of the RET proto-oncogene, were not detected in any of the examined cases of parathyroid tumors. These results suggest that mutations of the RET proto-oncogene do not represent a frequent mechanism of tumorigenesis for parathyroid tumors.
Mitsuo Itakura, Otsuka Department of Clinical and Molecular Nutrition, School of Medicine, The University of Tokushima, 3-18-15, Kuramoto-cho, Tokushima-city, 770 Japan
Effect of insulin and growth hormone on the synthesis of radiolabelled proteoglycans from cultured human arterial smooth-muscle cells
Authors: Thøgersen Vibeke B , Heickendorff Lene , Ledet Thomas 
Published: December 2008

Thogersen VB, Heickendorff L, Ledet T. Effect of insulin and growth hormone on the synthesis of radiolabelled proteoglycans from cultured human arterial smooth-muscle cells. Eur J Endocrinol 1996;134:326–30. ISSN 0804–4643
The present study focuses on the pathogenesis of increased frequency of large-vessel disease in diabetes. The diabetic arterial wall displays characteristic alterations of the extracellular matrix secreted by arterial smooth-muscle cells. The effects of insulin and growth hormone on the synthesis of sulphate-labelled proteoglycans and heparan sulphate proteoglycan were studied. Proteoglycans and heparan sulphate proteoglycan were obtained from the medium and the cell layer of cultured human arterial smooth-muscle cells grown in 5% human serum. Heparan sulphate proteoglycan was quantified using ethanol precipitation combined with specific enzyme degradation. Addition of insulin (0.01, 0.05 and 0.10 mU/ml) induced a significant accumulation of 35S-labelled proteoglycans in the cell layer (2p < 0.005 and 2p < 0.001). The relative amount of cell-associated heparan sulphate proteoglycan increased during insulin stimulation (2p < 0.05). Growth hormone stimulation (5.0 and 10.0 ng/ml) caused a significant decrease in the ratio between heparan sulphate proteoglycan and proteoglycan in the cell layer (2p < 0.02 and 2p < 0.01). whereas the distribution of proteoglycans between the cell layer and the medium was unaltered.
Vibeke Bech Thogersen, Research Laboratory for Biochemical Pathology, Department of Pathology, Aarhus University Hospital, Kommunehospitalet, Nørrebrogade 44, DK-8000, Aarhus C, Denmark
Enhanced expression of transforming growth factor β1 in rat thyroid hyperplasia is thyrotropin induced and time dependent
Authors: Morosini PP , Taccaliti A , Arnaldi G , Simonella G , Petrelli MD , Mancini V , Montironi R , Scarpelli M , Diamanti L , Mantero F 
Published: December 2008

Morosini PP, Taccaliti A, Arnaldi G, Simonella G, Petrelli MD, Mancini V, Montironi R, Scarpelli M. Diamanti L, Mantero F. Enhanced expression of transforming growth factor β1 in rat thyroid hyperplasia is thyrotropin induced and time dependent. Eur J Endocrinol 1996:134:373–8. ISSN 0804–4643
Forty-three 8-week-old male Wistar rats were studied to evaluate temporal changes of transforming growth factor β1 TGF-β1) mRNA levels in thyroid tissue during pharmacologically induced goiter. Four rats were treated with purified bovine thyrotropin (TSH; Ambinon, 2 mU/day sc) for 7 days before being sacrificed. Thirty-one were treated with propylthiouracil (PTU), added to their drinking water at a concentration of 0.2 g%, and subsequently were sacrificed as follows: five after 1 week PTU-1): five after 2 weeks PTU-2): five after 4 weeks PTU-4): five after 8 weeks PTU-8): five after 12 weeks (PTU-12). In six rats, after 12 weeks of treatment, PTU was withdrawn for 2 months and subsequently started again in three rats which were sacrificed after 2 weeks (PTU-R); the remaining three rats were sacrificed without any further treatment (PTU-R control). Eight rats (control rats) were never treated and served as controls. After sacrifice, blood was drawn for determination of total thyroxine and the thyroid was excised and subdivided into two lobes. Northern analysis for TGF-β1 was performed in one lobe, while histological and immunohistochemical studies were performed in the other lobe. Gene expression of TGF-β1 was induced in TSH- and PTU-treated rats. In TSH-treated rats TGF-β1 gene expression was less detectable than in PTU-treated rats, where it became evident after 2 weeks and remained through weeks 4–8. Gene expression of TGF-β1 was also seen in PTU-R rats, but not in the control and in the PTU-R control. Immunohistochemical analysis showed a different presence and location for the TGF-β1 protein, which appears to be dependent on the time of exposure to mitogenic stimulus. In conclusion, TGF-β1 is produced in response to both a direct (TSH by itself) and indirect (TSH induced by PTU-induced hypothyroidism) cellular proliferative stimulus and is not linked to an adaptative phenomenon secondary to hypothyroidism. The immunohistochemical location of TGF-β1 within the thyrocytes is influenced by mitogen exposure time. A TGF-β1 immunohistochemical evaluation may be important to define exposure time and activity of goitrogenic stimuli.
Pierpaolo Morosini, Clinica di Endocrinologia, c/o Ospedale Regionale, Via Conca, 60100 Torrette Ancona, Italy
Slowing of peripheral motor nerve conduction was ameliorated by aminoguanidine in streptozocin-induced diabetic rats
Authors: Miyauchi Yosuke , Shikama Hisataka , Takasu Toshiyuki , Okamiya Hideaki , Umeda Masako , Hirasaki Eiko , Ohhata Isao , Nakayama Hidetaka , Nakagawa Shoichi 
Published: December 2008

Miyauchi Y, Shikama H, Takasu T, Okamiya H, Umeda M, Hirasaki E, Ohhata I, Nakayama H, Nakagawa S. Slowing of peripheral motor nerve conduction was ameliorated by aminoguanidine in streptozocin-induced diabetic rats. Eur J Endocrinol 1996:134:467–73. ISSN 0804–4643
The aims of this study were to investigate the effect of aminoguanidine (AG) on slowing of motor nerve conduction velocity (MNCV) of the sciatic nerve in streptozocin-induced diabetic rats and to assess its mechanism of action. The MNCV of the sciatic nerve was measured electrophysiologically in diabetic rats treated with and without AG for 16 weeks. To elucidate the action of AG, morphological lesion and abnormality of polyol pathway metabolism in the nerve were examined and tissue levels of advanced glycosylation end-products (AGE) were determined as an indicator of AGE accumulation in tissue. Diabetic rats were treated with AG at three doses of 10, 25 and 50 mg/kg for 16 weeks. Myelinated fiber morphometry and nerve Na+,K+-ATPase activity were determined. The AGE levels in renal cortex were measured by a specific ELISA. Aminoguanidine dose-dependently ameliorated slowing of MNCV 16 weeks after the treatment without changing body weight or blood glucose levels. No difference in myelinated fiber morphometry or Na+,K+-ATPase activity with or without AG treatment was detected in diabetic rats. Diabetes increased the AGE level in the renal cortex by six times compared to non-diabetic rats, and AG reduced the rise in the AGE level by 40%. The MNCV was inversely correlated with the AGE levels. We conclude that improvement of conduction slowing by AG in experimental diabetes may be through decreasing the AGE level in the peripheral tissues. Aminoguanidine may have a therapeutic potential in controlling diabetic peripheral neuropathy.
Hisataka Shikama, Endocrinology and Metabolic Disease Research Laboratory, Yamanouchi Pharmaceutical Co., Ltd., 21 Miyukigaoka, Tsukuba, Ibaraki 305 Japan
Progesterone does not alter sympathetic activity in tissues involved in energy balance
Authors: Puerta Marisa , Venero César , Castro Carmen , Abelenda María 
Published: December 2008

Puerta M, Venero C, Castro C, Abelenda M. Progesterone does not alter sympathetic activity in tissues involved in energy balance. Eur J Endocrinol 1996;134:508–12. ISSN 0804–4643
Female rats acclimated to thermoneutrality to avoid cold influences received progesterone by means of subcutaneous implants. They increased their food intake and body weight above the values recorded in control animals. None the less, despite the enhanced food intake, no sign of activation of the sympathetic nervous system was observed, as judged by the unaltered noradrenaline content, half-life and turnover rate in brown adipose tissue, pancreas and heart. This indicates that progesterone increases food intake but prevents non-energy-conservation processes regulated by the sympathetic nervous system from taking place. Thus, it facilitates in two different ways the building up of energy stores. Because overfeeding induced by palatable diets increases the sympathetic tone to the organs studied, it is suggested that the central mechanisms regulating energy balance are probably influenced in a different manner by progesterone than by the sensory properties of palatable diets.
M Puerta, Departamento de Biología Animal II (Fisiología Animal), Facultad de Ciencias Biológicas, Universidad Complutense de Madrid, E-28040 Madrid, Spain
Selective macrophage depletion in the liver does not prevent the development of the sick euthyroid syndrome in the mouse
Authors: Boelen Anita , Schiphorst Marianne C Platvoet-ter , van Rooijen Nico , Wiersinga Wilmar M 
Published: December 2008

Boelen A, Platvoet-ter Schiphorst MC, van Rooijen N, Wiersinga WM. Selective macrophage depletion in the liver does not prevent the development of the sick euthyroid syndrome in the mouse. Eur J Endocrinol 1996;134:513–8. ISSN 0804–4643
A decreased serum triiodothyronine (T3) level is one of the main characteristics of the sick euthyroid syndrome, caused mainly by a decreased 5′-deiodination of thyroxine (T4) in the liver. Cytokines have been implicated in the pathogenesis of the changes in thyroid hormone metabolism during illness. We therefore investigated the role of cytokines produced by the liver macrophages (Kupffer cells) in the development of the sick euthyroid syndrome, which was induced in mice by a single injection of bacterial endotoxin (lipopolysaccharide) or by 24-h starvation. Experiments were carried out with or without previous selective depletion of liver macrophages by intravenous administration of liposome-encapsulated dichloromethylene diphosphonate. Relative to saline-injected pair-fed controls, the administration of lipopolysaccharide caused a decrease of serum T3 and T4 and liver 5′-deiodinase mRNA. Selective depletion of liver macrophages did not affect these changes. Starvation for 24 h decreased serum T3 and T4, associated with a slight decrease of liver 5′-deiodinase mRNA. There were no differences between macrophage-depleted and non-depleted animals in this respect. In summary, selective depletion of liver macrophages did not affect the decrease in serum T3, T4 or liver 5′-deiodinase mRNA induced by lipopolysaccharide or 24-h starvation in mice. We conclude that cytokines produced by Kupffer cells are not involved in the pathogenesis of the sick euthyroid syndrome in this experimental model.
A Boelen, Department of Endocrinology, F5-171 Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
Perinatal ontogeny of porcine growth hormone receptor gene expression is modulated by thyroid status
Authors: Duchamp C , Burton KA , Herpin P , Dauncey MJ 
Published: December 2008

Duchamp C, Burton KA, Herpin P, Dauncey MJ, Perinatal ontogeny of porcine growth hormone receptor gene expression is modulated by thyroid status. Eur J Endocrinol 1996;134:524–31
The ontogeny of growth hormone receptors (GHR) represents a critical stage in growth and metabolism. We have investigated the perinatal ontogeny of hepatic and skeletal muscle GHR gene expression in piglets, and its modulation by GH and thyroid hormones. Test piglets were rendered hypothyroid in late gestation by feeding the sow a high-glucosinolate rapeseed meal. Plasma and tissue samples were obtained from test and control piglets at various ages between 80 days of fetal life (80F) and 2 days postnatally. Plasma hormone levels were determined by radioimmunoassay and GHR mRNA by RNase protection assays. In controls, plasma thyroxine (T4) and 3,5,3′-triiodothyronine (T3) levels increased between 80F and birth and the early postnatal period was characterized by a marked surge in plasma T3. Test piglets were hypothyroid at 110F with total T4, total T3 and free T3 levels being reduced by 28, 53 and 33% respectively. By contrast, the postnatal increase in T3 was more marked in test than in control animals. Plasma GH levels decreased over the perinatal period and there was no effect of treatment. Hepatic GHR mRNA was at the lower limit of detection at 80F but by 11 OF was expressed in both groups of animals. However, fetal hypothyroidism at 11 OF resulted in a marked 70% decrease in hepatic GHR mRNA (p < 0.01). The higher postnatal rise in T3 in test piglets was accompanied by a recovery of hepatic GHR mRNA levels. By contrast with liver, skeletal muscle (longissimus dorsi) expressed high levels of GHR mRNA at 80F and hypothyroidism induced a 68% increase in GHR mRNA (p < 0.001). The present results suggest that thyroid hormones may modulate the perinatal ontogeny of GHR gene expression, in addition to other hormonal factors, and that this modulation is tissue-specific.
MJ Dauncey, Department of Cellular Physiology, The Babraham Institute, Cambridge CB2 4AT, UK
True insulin and intact proinsulin levels in acromegalic patients
Authors: Tavares Edelweiss F , Dalbosco Ivaldir S , Abucham Julio , Russo Ewaldo MK 
Published: December 2008

Tavares EF, Dalbosco IS, Abucham J, Russo EMK. True insulin and intact proinsulin levels in acromegalic patients. Eur J Endocrinol 1996;134:549–53. ISSN 0804–4643
To determine whether proinsulin (PI) contributes significantly to the immunoreactive insulin (IRI) concentrations in acromegalics, we measure PI, "true insulin" and IRI in a group of acromegalics compared with a control group. Serum PI was determined by the immunofluroimetric assay (IFMA). Insulin was also determined by an IFMA that measures true insulin and by a radioimmunoassay (RIA). We performed an oral glucose tolerance test (OGTT) in a total group of 46 subjects: 10 controls with normal OGTT and body mass index <25 kg/m2 (control group I), 10 controls with normal OGTT and body mass index > 25 kg/m2 (control group II), 15 patients with active acromegaly and normal OGTT and 11 patients with active acromegaly and IGT. Plasma glucose, serum GH, insulin and proinsulin were measured in all OGTT samples. Basal levels of insulin-like growth factor I (IGF-I) were measured in acromegalics. Mean body mass index in acromegalics with normal and impaired glucose tolerance were significantly higher compared with control group I and similar when compared with control group II. Proinsulin increased during OGTT in acromegalics with impaired glucose tolerance compared to control group I, and only fasting proinsulin compared to control group II. In normal OGTT acromegalics, only fasting proinsulin was increased. The RIA insulin during OGTT was significantly higher for both acromegalic groups compared to control group I and only at fasting when compared with control group II. This difference was not evident when insulin was measured by IFMA. These results suggest that in acromegalics, hyperinsulinism measured by RIA was at least in part due to hyperproinsulinism.
Ewaldo MK Russo, PO Box 20266, CEP 04034-970, Sáo Paulo, SP, Brazil