bluuebunny/crossref_metadata_2025_split huggingface dataset:
Response of triiodothyronine-dependent enzyme activities to insulin-like growth factor I and growth hormone in cultured rat hepatocytes
Authors: Pellizas Claudia G , Coleoni Aldo H , Cabanillas Ana M , Masini-Repiso Ana M , Costamagna María E 
Published: December 2008

Pellizas CG, Coleoni AH, Cabanillas AM, Masini-Repiso AM, Costamagna ME. Response of triiodothyronine-dependent enzyme activities to insulin-like growth factor I and growth hormone in cultured cat hepatocytes. Eur J Endocrinol 1996:134:215–20. ISSN 0804–4643
Triiodothyronine (T3) is involved in the regulation of the growth hormone-insulin-like growth factor I (GH-IGF-I) axis. In this study we investigated the effect of GH and IGF-I on the metabolic response of T3 in target tissues by evaluating the activity of two T3-dependent liver enzymes: mitochondrial α-glycerophosphate dehydrogenase (α-GPD) and cytosolic malic enzyme (ME) in rat hepatocytes in primary culture. Growth hormone (35 nmol/l) as well as IGF-I (0.5 μmol/l) reduced α-GPD and ME activities (p < 0.01) compared to the control group. Timecourse studies indicated that IGF-I 1.5 μmol/l) significantly decreased α-GPD and ME activities (p < 0.01) after 24 h, whereas the effect of GH (35 nmol/l) was recorded only after 36 h (p < 0.01). This delayed effect of GH compared to IGF-I suggested the possibility that the effect of GH could be mediated by IGF-I synthesis. To test this hypothesis, the effect of GH on the two enzyme activities was studied in the presence of anti-IGF-I antibodies. A gradual recovery of α-GPD and ME activities (p < 0.01) was observed in the presence of GH (35 nmol/l) plus increasing concentrations of anti-IGF-I antiserum. The maximal α-GPD and ME activities attained after the incubation of the liver cells with 1 μmol/l T3. a concentration high enough to fully saturate the nuclear T3 receptors for 24 h, were lowered significantly by 1.0 μmol/l IGF-I (p < 0.01). This finding suggests that the IGF-I effect might be independent of the saturation of the nuclear T3 receptors. In conclusion, in cultured rat hepatocytes, GH and IGF-I reduced the metabolic response of T3 evaluated by two liver T3-dependent enzyme activities. The effect of GH was mediated at least in part by IGF-I.
Claudia G Pellizas, Dpto Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Códoba, Casilla de Correo 61, Sucursal 16, (5016) Córdoba, Argentina.
Effects of 5,5′-diphenylhydantoin on the thyroid status in rats
Authors: Schröder-van der Elst JP , van der Heide D , van der Bent C , Kaptein E , Visser TJ , DiStefano JJ 
Published: December 2008

Schröder-van der Elst JP, van der Heide D, van der Bent C, Kaptein E, Visser TJ, DiStefano JJ, Effects of 5,5′diphenylhydantoin on the thyroid status in rats. Eur J Endocrinol 1996;134:221–4. ISSN 0804–4643
Treatment of rats with phenytoin (DPH), an anti-epileptic drug, results in lower tissue thyroid hormone (TH) levels. To investigate if this is accompanied by tissue hypothyroidism, rats were treated for 3 weeks with DPH (50 mg/kg body wt in food). Thyroid hormone-dependent parameters were measured, and the results were compared to those of control rats and to those of athyreotic rats substituted with thyroxine + triiodothyronine (Tx + TH) to reach the same plasma TH levels as DPH-treated rats. These rats were mildly hypothyroid with regard to their TH and TSH levels and TH-dependent parameters. Both DPH and Tx + TH led to a decrease in plasma thyroxine (T4) and triiodothyronine (T3) (±70% of the control). The percentage free T4 was unchanged. Plasma thyrotropin (TSH) was increased only in the Tx + TH rats (sixfold). For DPH rats, pituitary hormone content was not different from the control; growth hormone was lower and TSH was higher in Tx + TH rats. In DPH and Tx + TH rats, an increase in hepatic T4 and T3 uridine-diphosphate glucuronyltransferase activity was found, likewise indicating a change in the metabolic pathway of TH. Hepatic iodothyronine deiodinase (ID) type I activity decreased in Tx + TH rats but did not alter in DPH rats. Hepatic α-glycerophosphate dehydrogenase (α-GPD) decreased in DPH and Tx + TH rats. Malic enzyme in liver was enhanced in DPH rats. In the brains of DPH rats the level of α-GPD activity was raised; in Tx + TH it was lowered. The ID type II activity in the brain was reduced in DPH rats, but ID type III did not change for either group. Total body oxygen consumption increased in DPH rats (13%); it decreased in Tx + TH rats (9%). Our results show that DPH causes changes comparable to mild hypothyroidism. The lack of or a diminished hypothyroid response can be explained as the attenuating agonistic effect of DPH, which is supported by O2 consumption, brain ID type II and α-GPD activities. The T4 content was reduced by 30% in thyroid digests; this, together with a reduced T4 secretion, can lead to serious hypothyroxinemia during prolonged DPH treatment.
JP Schröder-van der Elst, Department of Metabolic Diseases and Endocrinology, Building 1, C4-R, University Hospital, Rijnsburgerweg 10, 2300 RC Leiden, The Netherlands
Progesterone together with estradiol promotes luteinizing hormone β-subunit mRNA stability in rat pituitary cells cultured in vitro
Authors: Park Deokbae , cheon Minseok , Kim Changmee , Kim Kyungjin , Ryu Kyungza 
Published: December 2008

Park D, Cheon M, Kim C, Kim K, Ryu K. Progesterone together with estradiol promotes luteinizing hormoneβ-subunit mRNA stability in rat pituitary cells in vitro. Eur J Endocrinol 1996;134:236–42. ISSN 0804–4643
The present study examined the role of ovarian steroids, estradiol and/or progesterone in the regulation of luteinizing hormone β-subunit (LH-β) mRNA levels and LH release in the rat anterior pituitary cells cultured in vitro. When estradiol (10 nmol/l and/or progesterone (100 nmol/l) were added to the cultures, neither estradiol or progesterone nor both together altered the basal LH-β mRNA levels or LH release. Continuous exposure to gonadotropin-releasing hormone (GnRH, 0.2 nmol/l) for 24 h markedly induced LH-β mRNA accumulation, and in this experimental condition, progesterone alone and progesterone + estradiol further augmented GnRH-induced LH-β mRNA levels and LH release. Then we explored further the possibility that ovarian steroids are involved in modulating LH-β mRNA stability in cultured rat pituitary cells where transcription was inhibited by actinomycin D. Anterior pituitary cells were preincubated with GnRH (0.2 nmol/l) for 16 h and, after removing GnRH from culture medium, the cells were incubated further in the presence of actinomycin D (5 μmol/l) for 24 h. The LH-β mRNA levels gradually declined to about 30% of the control values (zero time point after GnRH removal) in a time-dependent manner. During this period, either progesterone alone or progesterone + estradiol clearly blocked the degradation of LH-β mRNA species. These results indicate that ovarian steroids promote LH-β mRNA stability, thereby contributing to the maintenance of GnRH-stimulated LH-β mRNA levels.
Kyungza Ryu, Department of Pharmacology, College of Medicine, Yonsei University, 120-749, Seoul, Korea
Interleukin-1β-induced nitric oxide production from isolated rat islets is modulated by D-glucose and 3-isobutyl-1-methyl xanthine
Authors: Andersen Henrik U , Mauricio Dídac , Karlsen Allan E , Mandrup-Poulsen Thomas , Nielsen Jens H , Nerup Jørn 
Published: December 2008

Andersen HU, Mauricio D, Karlsen AE, Mandrup-Poulsen T, Nielsen JH, Nerup J. Interleukin-nitric oxide production from isolated rat islets is modulated by d-glucose and 3-isobutyl-1-methyl xanthine. Eur J Endocrinol 1996:134:251–9. ISSN 0804–4643
Interleukin-1β has been proposed to cause selective β-cell destruction via the induction of nitric oxide synthesis. The cytotoxic effect of interleukin-1β is modulated by the concentration of d-glucose in the medium. The aim of this study was to investigate if d-glucose-mediated modulation of interleukin-1β effects on insulin release from isolated rat islets was related to modulation of nitric oxide production. Further, we wished to investigate the effects of agents increasing the intracellular concentration of cAMP on interleukin-1β-induced nitrite production. We demonstrated that d-glucose potentiated interleukin-1β-induced nitrite production in rat islets without affecting the mRNA level of the inducible nitric oxide synthase. This effect was dissociated from interleukin-1β action on insulin release, since a relative protection against interleukin-1β effects on acute insulin release was found at high (28 mmol/l) concentrations of d-glucose, and blocking nitrite production by the L-arginine analog aminoguanidine, which selectively inhibits the cytokine-inducible nitric oxide synthase, did not result in protection against the inhibitory action of interleukin-1β Neither l-glucose nor the secretagogues l-leucine, tolbutamide and β-isobutyl-1-methyl xanthine shared the potentiating effect of d-glucose, The phosphodiesterase inhibitor β-isobutyl-1-methyl xanthine reduced interleukin-1β-induced nitrite production at 3.3 mmol/l d-glucose, an effect that could be reproduced by the cAMP analog dibutyryl cAMP. Addition of 3-isobutyl-1-methyl xanthine resulted in a threefold reduction in the mRNA level of interleukin-1β-induced inducible nitric oxide synthase. We conclude that interleukin-1β-induced islet nitric oxide synthesis is augmented by d-glucose but not by non-substrate secretagogues, and that secretagogues that elevate cAMP inhibit islet nitric oxide production.
Jørn Nerup, Steno Diabetes Center, Niels Steensens vej 2, DK-2820 Gentofte, Denmark
Relative value of computed tomography scanning and venous sampling in establishing the cause of primary hyperaldosteronism
Authors: Sheaves Richard , Goldin Jonathan , Reznek Rodney H , Chew Shern L , Dacie Janet E , Lowe David G , Ross Richard JM , Wass John AH , Besser G Michael , Grossman Ashley B 
Published: December 2008

Sheaves R, Goldin J, Reznek RH, Chew SL, Dacie JE, Lowe DG, Ross RJM, Wass JAH, Besser GM, Grossman AB, Relative value of computed tomography scanning and venous sampling in establishing the cause of primary hyperaldosteronism. Eur J Endocrinol 1996;134:308–13. ISSN 0804–4643
The purpose of this study was to evaluate the relative merits of the postural stimulation test, adrenal computed tomography (CT) and venous sampling in the differential diagnosis of patients presenting with primary hyperaldosteronism. The records of 20 patients presenting with primary hyperaldosteronism were reviewed retrospectively. There were 15 patients with a unilateral aldosterone-producing adenoma (APA), four patients with idiopathic hyperaldosteronism (IHA) and one patient with primary adrenal hyperplasia (PAH). The postural stimulation test was based on measurements of plasma aldosterone and renin activity at 08.00 h and at noon after 4 h of ambulation. The CT scans of the adrenals were reviewed by a single radiologist. Bilateral venous sampling of adrenal veins was attempted in all patients and blood collected for aldosterone and cortisol assay. Plasma aldosterone concentration increased after 4 h of standing in all cases of hyperplasia but was also demonstrated in 10/15 patients with a surgically-proven APA, If one defines a significant postural rise as being greater than 30%, then 8/15 patients with APA can be considered as being posturally responsive. Computed tomography scanning correctly identified all 15 cases of APA and also classified correctly the remaining five cases of hyperplasia (four cases of IHA and one case of PAH). Venous sampling failed technically in 4/15 cases of APA and in one case of IHA; a total of 5/20 (25%), A correct diagnosis of APA or IHA was established in all the remaining cases. However, the one case of PAH was treated successfully by adrenalectomy following venous sampling, which suggested a unilateral adrenal lesion: this one result was the only instance where venous sampling altered clinical decision-making. Computed tomography scanning may be used alone to confirm the cause of hyperaldosteronism where postural studies suggest an adrenal adenoma, and such patients may be considered for early surgery. Venous catheterization studies are not necessary routinely, but may still be useful in selected patients, particularly when CT scanning shows no clear lesion.
Ashley Grossman, Department of Endocrinology, St Bartholomew's Hospital, West Smithfield, London ECIA 7BE, UK
Increased plasma levels of islet amyloid polypeptide in patients with primary hyperparathyroidism
Authors: Valdemarsson Stig , Leckström Arnold , Westermark Per , Bergenfelz Anders 
Published: December 2008

Valdemarsson S, Leckström A, Westermark P, Bergenfelz A. Increased plasma levels of islet amyloid polypeptide in patients with primary hyperparathyroidism. Eur J Endocrinol 1996;134:320–5. ISSN 0804–4643
Amylin, also named islet amyloid polypeptide (IAPP), is a protein that is processed and released from pancreatic β-cells in parallel with insulin. Islet amyloid polypeptide is currently studied with regard to a role for insulin resistance in non-insulin-dependent diabetes. To elucidate a possible function of IAPP for impaired glucose tolerance in primary hyperparathyroidism (pHPT), we studied plasma IAPP levels during an oral glucose tolerance test (OGTT) in seven pHPT patients before and 8 weeks after surgery and in six healthy subjects. The β-glucose level of the patient groups was 4.34 ± 0.12 mmol/l before and 3.97 ± 0.16 mmol/l after surgery (NS), while the serum level of insulin was significantly higher before (16.9 ± 2.8 mIU/l) than after (8.9 ± 1.9 mIU/l) the operation (p < 0.05), indicating a moderately increased insulin resistance in pHPT. The basal plasma levels of IAPP were significantly higher in pHPT patients before than 8 weeks after surgery (9.71 ± 1.05 and 4.30 ± 0.82 pmol/l, respectively; p < 0.01). When compared to the plasma IAPP level of the controls at 1.80 ± 0.38 pmol/l, pHPT patients had higher IAPP values both before (p < 0.01) and at 8 weeks after (p < 0.05) operation, There was a significant correlation between the serum levels of insulin and plasma levels of IAPP in pHPT patients before (r = 0.87, p < 0.01) as wells as 8 weeks after surgery (r = 0.69, p < 0.05). The area under the curve for IAPP during OGTT in pHPT patients was 1872.4 ± 187.7 pmol·min/l, which is significantly higher than after surgery 1010.8 ± 93.7 pmol· min/l) (p < 0.05) and compared to the area for the controls at 840.3 ± 49.9 pmol min/l (p< 0.01). In conclusion, pHPT is associated with an increased plasma level of IAPP, correlated to the serum insulin level, but persistently higher than in controls also 8 weeks after surgery. Possibly, increased IAPP levels can have a role for impaired glucose tolerance in pHPT. The hyperparathyroid state might have a specific role for the release of this peptide, otherwise closely connected to insulin secretion.
Stig Valdemarsson, Department of Internal Medicine, Lund University Hospital, S-221 85 Lund, Sweden
Peptide YY does not inhibit glucose-stimulated insulin secretion in humans
Authors: Ahrén Bo , Larsson Hillevi 
Published: December 2008

Ahrén B, Larsson H. Peptide YY does not inhibit glucose-stimulated insulin secretion in humans. Eur J Endocrinol 1996;134:362–5. ISSN 0804–4643
Peptide YY (PYY) is localized to gut and pancreatic endocrine cells. It may therefore be involved in the regulation of insulin secretion as a gut hormone as well as an islet local regulator. In laboratory animals, the peptide inhibits stimulated insulin secretion, but its effects in humans are not known. We therefore infused PYY intravenously at a low (1 pmol·kg−1 · min−1; N = 4) or a high rate (5 pmol · kg−1 · min−1; N= 5) for 120 min in healthy women aged 52 years. After 30 min of infusion, glucose (0.5 g/kg) was injected rapidly. In separate control experiments, saline was infused instead of PYY. We found that PYY did not inhibit the acute insulin response to glucose or affect the glucose elimination rate, and PYY was also without influence on the basal plasma glucose and serum insulin levels during the 30-min infusion before the challenge with glucose. We therefore conclude that intravenous infusion of PYY does not affect glucose-stimulated insulin secretion in man.
Bo Ahrén, Department of Medicine, Malmö University Hospital, S-205 02 Malmö, Sweden
Differential subcellular distribution of rat prostatic steroid 5α-reductase isozyme activities
Authors: Span Paul N , Sweep CGJ , Benraad Theo J , Smals Anthony GH 
Published: December 2008

Span PN, Sweep CGJ, Benraad TJ, Smals AGH. Differential subcellular distribution of rat prostatic steroid 5α-reductase isozyme activities. Eur J Endocrinol 1996;134:386–92. ISSN 0804–4643
The rat prostate, a classical androgen-target tissue, contains both known isozymes of steroid 5α-reductase, i.e. type I and type II. So far, the role of the type I isozyme has been proposed as catabolic. The abundant expression of type I 5α-reductase in an androgen-target tissue is therefore puzzling. Assessment of the subcellular localization of 5α-reductase isozymes in rat prostate might contribute in elucidating their possibly distinct roles. After obtaining crude subcellular fractions by differential centrifugation, both isozyme activities were measured at neutral pH by plotting according to Eadie–Scatchard. The observations were extended by assessment of pH-dependent velocity ratios and type II 5α-reductase inhibitor sensitivities in these subcellular fractions. The results indicated a preferentially—although not exclusively—nuclear localization for the type I and a predominantly microsomal localization for the type II isozyme activity in the rat prostate. In conclusion, the nuclear localization of the type I isozyme seems not to concur with its proposed catabolic role.
AGH Smals, Department of Medicine, Division of Endocrinology, University Hospital Nijmegen, Geert Grooteplein Zuid 8, 6525 GA Nijmegen, The Netherlands
Major histocompatibility complex class II and complement polymorphisms in postpartum thyroiditis
Authors: Parkes Arthur B , Darke Christopher , Othman Sakinah , Thomas Melanie , Young Neil , Richards Colin J , Hall Reginald , Lazarus John H 
Published: December 2008

Parkes AB, Darke C, Othman S, Thomas M, Young N, Richards CJ, Hall R, Lazarus JH. Major histocompatibility complex class II and complement polymorphisms in postpartum thyroiditis. Eur J Endocrinol 1996;134:449–53. ISSN 0804–4643
The objective was to re-evaluate the association between class II HLA-DR and DQ MHC antigens and postpartum thyroiditis (PPT) and to determine the prevalence of the class III complement allotypes of Properdin factor B (Bf), C4A and C4B in this condition. Two hundred and sixty-five (of 2897) pregnant women screened positive for thyroid autoantibody activity took part. Further blood samples were obtained for HLA class II (185) and complement (193) typing. The severity of the ensuing PPT was assessed by measuring thyroid function during the postpartum year. The HLA-DR and DQ phenotypes were assigned from restriction fragment length polymorphism analysis, and Bf, C4A and C4B allotypes were determined by immunofixation with anti-Bf or anti-C4 antibodies after electrophoresis. A weak association between the HLA class II antigens and PPT, as indicated by a reduced frequency of DR15 and DQ6 together with an increased frequency of DR5 and DQ7. was confirmed. However, only the change in DR5 frequency remained significant after correction (corrected p < 0.05). Postpartum thyroiditis was also associated with frequency disturbances in Bf and C4A allotypes but not C4B allotypes. Whilst this study has not provided evidence of a strong marker gene for PPT, it does not preclude the involvement of the MHC in this condition. These data show disturbances in complement allotype frequencies, suggesting that the class III region may provide a useful focus for further study of this pathology.
AB Parkes, Autoimmunology Research Unit, Section of Endocrinology, Metabolism and Diabetes, Department of Medicine, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XN, UK
Effects of the dopamine agonist cabergoline in patients with prolactinoma intolerant or resistant to bromocriptine
Authors: Delgrange Etienne , Maiter Dominique , Donckier Julian 
Published: December 2008

Delgrange E, Maiter D, Donckier J. Effects of the dopamine agonist cabergoline in patients with prolactinoma intolerant or resistant to bromocriptine. Eur J Endocrinol 1996;134:454–6. ISSN 0804–4643
Cabergoline is a new long-acting ergoline derivative used to treat hyperprolactinaemia. Its effect was assessed in 10 patients (eight women and two men) with prolactinoma who were intolerant (group I; N = 7) or resistant (group II; N = 3) to bromocriptine. In group I, no side effect was observed on cabergoline therapy; two patients became pregnant and normoprolactinaemia was achieved in the five others. In group II, cabergoline was active and well-tolerated in two out of the three patients: one woman had three consecutive pregnancies; in another patient normoprolactinaemia was restored and the tumour shrank by 60%; in the third patient cabergoline was discontinued because of side effects and inefficacy. Thus, cabergoline appears to be an alternative of choice as treatment of hyper-prolactinaemic patients who are intolerant or resistant to bromocriptine.
Julian Donckier, Internal Medicine and Endocrinology, University Hospital UCL of Mont-Godinne, B-5530 Yvoir, Belgium
Insulin treatment fails to abolish the teratogenic potential of serum from diabetic rats
Authors: Wentzel Parri , Eriksson Ulf J 
Published: December 2008

Wentzel P, Eriksson UJ. Insulin treatment fails to abolish the teratogenic potential of serum from diabetic rats. Eur J Endocrinol 1996;134:459–66. ISSN 0804–4643
Maternal diabetes during pregnancy constitutes an increased risk for congenital malformations in the offspring. Previous studies have identified several serum components with teratogenic activity, e.g. glucose and β-hydroxybutyrate, but have also suggested that the teratogenic influence of the diabetic environment on the developing embryo is multifactorial and may depend upon changed concentrations of several maternal metabolites. In the present investigation we aimed to assess the teratological impact of small, concomitant alterations in a series of metabolites, particularly those not previously identified as teratogens. We thus investigated the influence of a mild diabetic environment by culturing gestational day-9 rat embryos in serum from insulin-treated diabetic rats for 48 h in vitro, and compared the embryonic outcome with that obtained after culture in normal serum and in serum from manifestly diabetic rats without insulin treatment. The glucose concentration was adjusted to 10 or 30 mmol/l in the cultures, and the embryos were evaluated with respect to crown–rump length, protein and DNA content, number of somites and malformation score (comparing major, minor or no malformations). We found that increased glucose levels caused embryonic maldevelopment in both normal and diabetic serum, and that despite normalization of the diabetic state, the serum from the insulin-treated diabetic rats caused more growth retardation than the nondiabetic control serum. The normalized diabetic serum was also more teratogenic than the normal serum at the low glucose concentration, whereas the serum from the manifestly diabetic rats tended to cause more dysmorphogenesis at 30 mmol/l glucose than both the normal and normalized diabetic serum. The results suggest that the teratogenicity of maternal serum in diabetic pregnancy is not mediated exclusively by increased concentrations of glucose and ketone bodies. The efforts to diminish the teratogenic effects of a diabetic environment should therefore include normalization of a multitude of serum factors, including glucose and ketone bodies.
Parri Wentzel, Department of Medical Cell Biology, University of Uppsala, Biomedicum, PO Box 571, S-751 23 Uppsala, Sweden