bluuebunny/crossref_metadata_2025_split huggingface dataset:
Corticotrophin-releasing hormone and β-endorphin in labour
Authors: McLean Mark , Thompson David , Zhang Hong-Ping , Brinsmead Max , Smith Roger 
Published: December 2008

McLean M, Thompson D, Zhang H-P, Brinsmead M, Smith R. Corticotrophin-releasing hormone and β-endorphin in labour. Eur J Endocrinol 1994;131:167–72. ISSN 0804–4643
The objectives of this study were to determine whether the maternal plasma corticotrophin-releasing hormone (CRH) concentration influences the amount of uterine contractility induced by infused oxytocin during induction of labour, and secondly to assess changes in CRH and β-endorphin in response to stress during labour. Serial plasma CRH and β-endorphin measurements were made in 40 women undergoing induction of labour and correlated with uterine contractility, cervical dilatation, length of labour, analgesic usage and fetal distress. The plasma CRH concentration did not change throughout labour. In subjects receiving infused oxytocin there was a significant positive correlation between plasma CRH and the amount of uterine activity, and a high plasma CRH level was associated with shorter labour. The plasma β-endorphin level rose with progressive cervical dilatation and fell after epidural anaesthesia. The plasma CRH level did not correlate with the plasma β-endorphin level or rise with fetal distress. We conclude that high levels of maternal plasma CRH are associated with an increase in the uterine contractile response to infused oxytocin. The maternal plasma CRH level does not vary in response to maternal or fetal stress, but β-endorphin secretion does rise in response to the stress of labour and is influenced by pain perception.
Mark McLean, Endocrine Unit, John Hunter Hospital, Locked Bag 1, Newcastle Mail Centre, Newcastle, NSW 2310, Australia
Abnormalities in the renin–angiotensin–aldosterone system in normotensive subjects with a positive family history of hypertension
Authors: Herlitz Hans , Widgren Bengt , Wikstrand John , Aurell Mattias 
Published: December 2008

Herlitz H, Widgren B, Wikstrand J, Aurell M, Abnormalities in the renin–angiotensin–aldosterone system in normotensive subjects with a positive family history of hypertension. Eur J Endocrinol 1994:131:179–83. ISSN 0804–4643
Non-hypertensive men with a positive family history of hypertension in two generations (N = 16) were compared with weight-matched (N = 13) and lean (N = 12) control groups with a negative family history of hypertension with respect to the activity of the renin–angiotensin–aldosterone system at baseline and during an oral glucose tolerance test. Blood pressure was measured phonographically after 30 min of semirecumbent rest and the oral glucose tolerance test was performed after a 10-h overnight fast with 100 g of glucose given orally. Blood samples were drawn from a peripheral catheter at baseline, 30 and 120 min after the glucose challenge. Systolic and diastolic blood pressures did not differ between subjects with a positive or a negative family history of hypertension. At baseline, blood glucose and plasma insulin were similar in the three groups while the group with a positive family history of hypertension had a significantly lower plasma renin activity (PRA) (0.85 ± 0.09 compared with the weight-matched but not with the lean control group (1.36 ± 0.13 and 1.06 ± 0.15 ng AI·ml−1 · h−1; p < 0.01 and NS, respectively). The PRA increased significantly after the glucose challenge in all groups (p < 0.01), while the plasma aldosterone concentration decreased after 30 min and then showed an increase at 120 min. The PRA response was less pronounced in the group with a positive family history of hypertension compared with the weight-matched and lean control groups (p < 0.05 and p < 0.01, respectively). Serum potassium did not change significantly in either group after the glucose challenge. Urinary sodium excretion was similar in the three groups. In conclusion, non-hypertensive subjects with a positive family history of hypertension are characterized by a lower activity of the renin–angiotensin–aldosterone system at baseline and a diminished PRA response during hyperinsulinemia compared with normotensive individuals without such heredity. Whether this is due to volume expansion or to a tendency to a higher blood pressure remains to be clarified.
Hans Herlitz, Department of Nephrology, Sahlgrenska sjukhuset, S-413 45 Göteborg, Sweden
Association of a nocturnal rise in plasma α-atrial natriuretic peptide and reversed diurnal blood pressure rhythm in hospitalized normotensive subjects with non-insulin dependent diabetes mellitus
Authors: Nakano Shigeru , Uchida Kenzo , Ishii Takashi , Takeuchi Mihoko , Azukizawa Sadahide , Kigoshi Toshikazu , Morimoto Shinpei 
Published: December 2008

Nakano S, Uchida K, Ishii T, Takeuchi M, Azukizawa S, Kigoshi T, Morimoto S. Association of a nocturnal rise in plasma alpha-atrial natriuretic peptide and reversed diurnal blood pressure rhythm in hospitalized normotensive subjects with non-insulin dependent diabetes mellitus. Eur J Endocrinol 1994;131:184–90. ISSN 0804–4643
Diurnal changes in plasma atrial natriuretic peptide (ANP), plasma renin activity (PRA) and plasma aldosterone as related to those in blood pressure (BP) were studied under hospital conditions in 18 diabetic subjects without proteinuria and 8 age-matched control subjects. Of 18 diabetic subjects, 10 had a normal diurnal BP rhythm with the peak value in the afternoon (group 1) and 8 had a reversed BP rhythm with the peak value during the night (group 2). Autonomic dysfunction estimated by measuring orthostatic BP and heart-rate changes and beat-to-beat heart-rate variations was more pronounced in group 2 than in group 1. Fasting plasma glucose and HbA1c were similarly high in both diabetic groups. Group 1 showed modestly elevated mean 24-h MBP and plasma ANP levels, modestly low mean 24-h PRA and plasma aldosterone levels, and a lack of diurnal ANP changes similar to that in controls. Group 2 showed markedly elevated mean 24-h BP and plasma ANP levels, markedly low mean 24-h PRA and plasma aldosterone levels, and nocturnal rises in plasma ANP and BP. PRA and plasma aldosterone exhibited circadian rhythms with their peak values found in the early morning in all three groups. The daytime/overnight excretion ratios of sodium and water were normal in group 1 and low in group 2. These results indicate that diurnal changes in plasma ANP, PRA and plasma aldosterone are altered in diabetic subjects with normal and reversed diurnal BP rhythms, predominantly in the latter.
Shigeru Nakano, Division of Endocrinology, Department of Internal Medicine, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Ishikawa 920-02, Japan
Inhibition by rat diazepam-binding inhibitor/acyl-CoA-binding protein of glucose-induced insulin secretion in the rat
Authors: Östenson Claes-Göran , Ahrén Bo , Karlsson Sven , Knudsen Jens , Efendic Suad 
Published: December 2008

Östenson C-G, Ahrén B, Karlsson S, Knudsen J, Efendic S. Inhibition by rat diazepam-binding inhibitor/ acyl-CoA-binding protein of glucose-induced insulin secretion in the rat. Eur J Endocrinol 1994;131:201–4. ISSN 0804–4643
Diazepam-binding inhibitor (DBI) has been localized immunohistochemically in many organs. In porcine and rat pancreas, DBI is present in non-B-cells of the pancreatic islets. Porcine peptide also has been shown to suppress insulin secretion from rat pancreas in vitro. Recently, acyl-CoA-binding protein (ACBP) was isolated from rat liver and shown to be identical structurally to DBI isolated from rat brain. Using this rat DBI/ACBP, we have studied its effects on glucose-stimulated insulin secretion in the rat, both in vivo and in isolated pancreatic islets. Infusion iv of rDBI/ACBP (25 pmol/min) during glucose stimulation induced a moderate and transient reduction of plasma insulin levels. Moreover, rDBI/ACBP suppressed insulin release from batch-incubated isolated islets, stimulated by 16.7 mmol/l glucose, by 24% at 10 nmol/l (p < 0.05) and by 40% at 100 nmol/l (p < 0.01). The peptide (100 nmol/l) also inhibited the insulin response to glucose (16.7 mmol/l) from perifused rat islets by 31% (p < 0.05), mainly by affecting the acute-phase response. Finally, incubation of isolated islets in the presence of rDBI/ACBP antiserum (diluted 1:100 and 1:300) augmented the insulin response to 16.7 mmol/l glucose (p < 0.05 or even less). We conclude that rDBI/ACBP, administered iv or added to the incubation media, suppresses insulin secretion in the rat but that the effect is moderate despite the high concentration used. It is therefore unlikely that the peptide modulates islet hormone release, acting as a classical hormone via the circulation. However, the occurrence of DBI/ACBP in the islets and the enhancing effect by the rDBI/ACBP antibodies on glucose-stimulated insulin release suggest that the peptide is a local modulator of insulin secretion.
C-G Östenson, Department of Endocrinology, Karolinska Hospital, S-171 76 Stockholm, Sweden
Effect of growth hormone treatment on insulin secretion and glucose metabolism in prepubertal boys with short stature
Authors: Åman Jan , Rosberg Sten , Albertsson-Wikland Kerstin 
Published: December 2008

Aman J. Rosberg S, Albertsson-Wikland K. Effect of growth hormone treatment on insulin secretion and glucose metabolism in prepubertal boys with short stature. Eur Endocrinol 1994;131:246–50. ISSN 0804–4643
The purpose of this study was to evaluate the effect on insulin secretion and glucose metabolism of daily growth hormone (GH) treatment, 0.1 U/kg. for up to 3 years in 42 short prepubertal boys without GH deficiency. Their median height standard deviation (sd) score increased from −2.7 to −1.7, whereas their weight for height sd score was unchanged after 3 years of treatment. Fasting plasma glucose concentrations were unchanged, but median fasting insulin concentrations increased from 6.0 mU/l before treatment to 7.8 mU/l (p < 0.05) after the first year. No further increase was seen during the second or third years. The median insulin area under the curve 10–60 min after an intravenous glucose tolerance test increased from 480 mU·1−1·min−1 before treatment to 799 mU·1−1 · min−1 (p < 0.05) after 1 year. The median glucose disposal rate (K value) before GH treatment, 2.2%/min, was unchanged after 1 year of treatment. A significant positive correlation was found between the change in the height sd score and the change in fasting insulin concentration during the first (r = 0.45; p < 0.01) and second (r = 0.56; p < 0.05) years of GH treatment. It was concluded that GH treatment in prepubertal children without GH deficiency caused a moderate increase in fasting and stimulated insulin concentrations during the first year of treatment. There was no further change during the following years of treatment, and there were no negative effects on fasting plasma glucose concentrations or glucose disposal rates. The increase in insulin concentration was related positively to the growth response.
Jan Åman, Department of Pediatrics, Örebro Medical Centre Hospital, S-701 85 Örebro, Sweden
Beneficial metabolic effects of insulin-like growth factor I in patients with severe insulin-resistant diabetes type A
Authors: Zenobi Peter D , Glatz Yvonne , Keller Annamarie , Graf Susanne , Jaeggi-Groisman Silvia E , Riesen Walter F , Schoenle Eugen J , Froesch E Rudolf 
Published: December 2008

Zenobi PD, Glatz Y, Keller A, Graf S, Jaeggi-Groisman SE, Riesen WF, Schoenle EJ, Froesch ER. Beneficial metabolic effects of insulin-like growth factor I in patients with severe insulin-resistant diabetes type A. Eur J Endocrinol 1994;131:251–7. ISSN 0804–4643
Severe insulin resistance type A is due to mutations in the insulin receptor gene and is characterized by glucose intolerance or diabetes mellitus, despite extreme hyperinsulinemia, virilization and acanthosis nigricans. At present, there is no therapy for this condition. Recently, we showed that glucose levels in three such patients are promptly lowered by an iv bolus of recombinant human insulin-like growth factor I (rhIGF-I). In the present study, we investigated two of these rare patients again and determined fasting and postprandial glucose, insulin, C-peptide, proinsulin and lipid levels during five control, five treatment and three wash-out days while on a constant diet. Treatment consisted of 2 × 150 μg rhIGF-I/kg sc per day, which elevated total IGF-I levels 4.5-fold above the control. Fasting glucose levels (days 1–5) in the two patients were 9.6±1.3 and 9.2 ± 1.2 mmol/l, respectively, and fell to 4.4±0.4 and 5.1±0.5 mmol/l on treatment days 8–10. Fasting insulin (2950±450 and 690±125 pmol/l), C-peptide (2217±183 and 1317±235 pmol/l) and proinsulin control levels (125±35 and 66±0 pmol/l) also decreased by ~65% during rhIGH-I treatment, as did the respective postprandial levels. Lipid levels hardly changed at all. In conclusion, IGF-I appears to correct partially some metabolic sequelae of severe insulin resistance and may, hence, be used as a new therapeutic agent.
E Rudolf Froesch, Department of Internal Medicine, University Hospital, Rämistrasse 100, 8091 Zurich, Switzerland
Secretion pattern of immunoreactive inhibin in men
Authors: Brennemann Wolfgang , Sommer Lieselotte , Stoffel-Wagner Birgit , Bidlingmaier Frank , Klingmüller Dietrich 
Published: December 2008

Brennemann W, Sommer L, Stoffel-Wagner B, Bidlingmaier F, Klingmüller D. Secretion pattern of immunoreactive inhibin in men. Eur J Endocrinol 1994;131:273–9. ISSN 0804–4643
Chronological changes in serum concentrations of inhibin, a gonadal glycoprotein hormone, were studied in healthy male volunteers (age 24–27 years). Secretion profiles of immunoreactive inhibin (ir-inhibin) were compared with those of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone. Blood samples were collected every 15 min for 24 h. Serum inhibin concentrations were measured by a two-site immunoenzymatic assay with antibodies raised against distinct epitopes of the recombinant 1–32 amino acids of the α-subunit of human inhibin. The normal range for men was 0.79–3.1 U/l × 10−3, the sensitivity of the assay was 0.1 U/l × 10−3 (cv: within-assay, 6.8%; between-assay, 8.2%). Luteinizing hormone and FSH were measured by immunoradiometric assay and testosterone by radioimmunoassay. Secretion profiles of inhibin and testosterone were tested for diurnal variations by cosinor rhythmometry. Highest ir-inhibin concentrations were observed in the morning at 08.00 h, with peak values of 2.45–3.20 U/l × 10−3. During the evening and the night, ir-inhibin levels were relatively low; lowest concentrations were observed between 01.00 h and 02.00 h at night: 1.20–1.86 U/l × 10−3. Highest testosterone levels were observed in the morning (20.5–36.6 pmol/I), lowest concentrations were detected at night (7.35–12.6 pmol/l). Cosinor rhythmometry supported the suggestion that there is a clear circadian secretion of ir-inhibin and testosterone, respectively. The secretion pattern of ir-inhibin was analyzed by the Cluster pulse analysis computed algorithm, which identified four to seven inhibin pulses per day, depending on the person under observation. A significant correlation could be observed between median testosterone and ir-inhibin concentrations (r = 0.449, p < 0.001). In conclusion, ir-inhibin and testosterone in healthy male volunteers follow a clear diurnal rhythm. Moment to moment changes of ir-inhibin can be observed in all secretion profiles investigated. A probable physiological role for pulsatile inhibin secretion is not yet clarified.
Dietrich Klingmüller, Institut für Klinische Biochemie, Universität Bonn, Sigmund-Freud-Str. 25, D-53105 Bonn, Germany
Interleukin 1β, tumor necrosis factor-α and interleukin 6 decrease nuclear thyroid hormone receptor capacity in a liver cell line
Authors: Wolf Matthias , Hansen Nils , Greten Heiner 
Published: December 2008

Wolf M, Hansen N, Greten H. Interleukin 1β, tumor necrosis factor-α and interleukin 6 decrease nuclear thyroid hormone receptor capacity in a liver cell line. Eur J Endocrinol 1994;131:307–12. ISSN 0804–4643
Many of the acute inflammatory responses in critical illness are mediated by tumor necrosis factor-α (TNF-α), interleukin 1/3 (IL-1β) and interleukin 6 (IL-6). Furthermore, these cytokines are involved in mediating the characteristic changes of thyroid function during acute disease known as non-thyroidal illness. In the present studies we investigated in vitro whether TNF-α, IL-1β and IL-6 modify nuclear thyroid hormone receptor (TR) capacity and/or affinity. Regulation of TR synthesis was studied in the human hepatoma cell line Hep-G2. Subconfluent cells were incubated with recombinant cytokines in serum-free medium. Nuclear extracts were prepared by high-salt extraction of cell nuclei. Binding assays were performed with [125I]-triiodothyronine; bound and free hormone were separated by filtration. Interleukin 1β decreased TR capacity in a dose-dependent manner. Compared with unstimulated cells, the TR capacity was reduced to 87.9 ± 3.9% (p < 0.05), 80.1 ± 3.9% (p < 0.01) and 72.1 ± 5.1% (p < 0.01) after incubation with 0.1,1.0 and 100 μg/l IL-1β respectively. Interleukin 6 and TNF-α significantly reduced receptor capacity only at concentrations of 10 μg/l or higher and the magnitude of the reduction was lower than with IL-1β. The TR capacity was reduced to 81.2 ± 2.3% (p < 0.01) and 83.2 ± 6.6% (p < 0.05) after stimulation with 10 μg/l IL-6 or TNF-α. respectively. TR affinity was not altered significantly after stimulation with any of the cytokines. In conclusion, we present evidence that the capacity of hepatic nuclear TRs is regulated by IL-1β. IL-6 and TNF-α. As cellular reaction to thyroid hormone stimulation depends on the number of nuclear TRs, this mechanism may serve to restrict catabolic effects of thyroid hormones during acute illness.
M Wolf, Medizinische Kern- und Poliklinik, Universitäts-Krankenhaus Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany
Follicle-stimulating hormone regulation of inhibin α-subunit mRNA in staged rat seminiferous tubules
Authors: Kaipia Antti , Penttilä Tarja-Leena , Toppari Jorma 
Published: December 2008

Kaipia A, Penttilä T-L, ToppariJ. Follicle-stimulating hormone regulation of inhibin α-subunit mRNA in staged rat seminiferous tubules. Eur J Endocrinol 1994;131:323–9. ISSN 0804–4643
Steady-state levels of inhibin-α and -βB mRNAs are higher in stages II–VI of the seminiferous epithelial cycle than in stages VII–VIII We investigated follicle-stimulating hormone (FSH) regulation of inhibin α-subunit mRNA in stages II–VI and VII–VIII to study whether the stage specificity is due to differential hormonal regulation by FSH. Follicle-stimulating hormone caused a significant increase of inhibin-α mRNA levels in both stages during a 20-h incubation. The mechanism of the FSH effect was studied further in stages VII-VIII. Maximal stimulation of the inhibin-α mRNA level was achieved with 100 μg/l FSH, dibutyryl-3′,5′-cyclic adenosine monophosphate (db-cAMP, 0.2 mmol/l) and Spadenosine-3′,5′-monophosphothionate (Sp-cAMPS, 10 μmol/l) (a cAMP agonist). The presence of RpcAMPS (200 μmol/l) (a cAMP antagonist) abolished the stimulation, Rp-cAMPS alone had no effect. inhibin-βB mRNA levels in stages VII–VIII were not affected by FSH, db-cAMP, Sp-cAMPS or Rp-cAMPS. Phorbol 12-myristate 13-acetate (100 nmol/l) had no effect on inhibin-α or -βB mRNA levels. Actinomycin D abolished the stimulatory effect of FSH on inhibin-α mRNA expression. In conclusion, FSH stimulated inhibin-α mRNA expression similarly both in stages II–VI and VII–VIII of the seminiferous epithelial cycle and the stimulation in stages VII–VIII was cAMP-mediated.
Jorma Toppari, University of Turku, Institute of Biomedicine, Department of Physiology, Kiinamyllynkatu 10, FIN-20520 Turku, Finland
Variable biological activity of thyroid-stimulating hormone
Authors: Beck-Peccoz Paolo , Persani Luca 
Published: December 2008

Beck-Peccoz P, Persani L. Variable biological activity of thyroid-stimulating hormone. Eur J Endocrinol 1994;131:331–40. ISSN 0804–4643
Thyroid-stimulating hormone (TSH), like the other pituitary glycoprotein hormones, is produced and secreted as a mixture of isoforms, the majority of which represent differences in oligosaccharide structure and possess different bioactivity. When samples are quantified simultaneously by immunometric assay and bioassay, the ratio between bioactivity (B) and immunoreactivity (I) may serve as an index of the overall potency of TSH. Variations of the TSH B/I ratio have been documented in both physiological and pathological conditions associated with alteration of the two most important mechanisms controlling TSH synthesis and secretion, i.e. TRH release and the thyroid hormone feedback system. Major examples of this assumption are the low TSH bioactivity found in samples from patients lacking TRH and thus bearing a hypothalamic hypothyroidism, and the enhanced bioactivity that is invariably found in TSH from patients with thyroid hormone resistance. Moreover, variations of TSH bioactivity have been recorded in normal subjects during the nocturnal TSH surge, in normal fetuses during the last trimester of pregnancy, in patients with primary hypothyroidism and in patients with TSH-secreting pituitary adenoma and non-thyroidal illness. In conclusion, the secretion of TSH molecules with altered bioactivity plays an important pathogenetic role in various thyroid disorders, while in some particular physiological conditions the bioactivity of TSH may vary in order to adjust thyroid hormone secretion to temporary needs.
Paolo Beck-Peccoz, Istituto di Scienze Endocrine, Ospedale Maggiore IRCCS, Via F. Sforza 35, 1-20122 Milano, Italy
Recombinant growth hormone and insulin-like growth factor I do not alter gonadotrophin stimulation of the baboon testis in vivo
Authors: Crawford Bronwyn A , Handelsman David J 
Published: December 2008

Crawford BA, Handelsman DJ. Recombinant growth hormone and insulin-like growth factor I do not alter gonadotrophin stimulation of the baboon testis in vivo. Eur J Endocrinol 1994;131:405–12. ISSN 0804–4643
In vitro studies indicate a physiological role for insulin-like growth factor I (IGF-I) in paracrine regulation of testicular function and recent clinical studies suggest a potential role for growth hormone (GH) and/or IGF-I in the treatment of hypogonadotrophic states in males. This study aimed to examine the effects of pretreatment with recombinant human GH (rhGH) or rhIGF-I on the response to gonadotrophins of the non-human primate testis in vivo. Using a balanced Latin square design with repeated measures, six prepubertal male hamadryas baboons (Papio hamadryas hamadryas) were treated in a cross-over sequence for periods of 18 days with daily im injections of rhGH (0.4 IU·kg−1 · day−1), rhIGF-I (0.1 mg·kg−1 · day−1) or saline with a 2-week washout period between each treatment. A single im injection of hCG (1500 IU) increased serum testosterone (p = 0.0002) but neither rhGH nor rhIGF-I influenced the timing or magnitude of this response (p > 0.5). A single im dose of FSH (75 IU) stimulated immunoreactive inhibin (p = 0.01) but also was unaffected in magnitude or timing by pretreatment with rhGH or rhIGF-I (p> 0.2). Circulating IGF-I levels were increased independently by hCG (p = 0.01) and FSH (p < 0.0001) administration. These findings indicate that neither GH nor IGF-I pre-treatment enhance acute gonadal responses to gonadotrophin stimulation of the prepubertal non-human primate testis in vivo. These findings suggest that GH or IGF-I treatment of hypogonadotrophic men without somatotrophin deficiency is unlikely to be beneficial.
David J Handelsman, Andrology Unit, Royal Prince Alfred Hospital, Departments of Medicine and Obstetrics and Gynaecology, University of Sydney, Sydney 2006, Australia