bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serum leptin and weight reduction in female obesity
Authors: Geldszus R , Mayr B , Horn R , Geisthövel F , von zur Mühlen A , Brabant G 
Published: December 2008

Geldszus R, Mayr B, Horn R, Geisthövel F, von zur Mühlen A, Brabant G. Serum leptin and weight reduction in female obesity. Eur J Endocrinol 1996;135:659–62. ISSN 0804–4643
Leptin, an adipocyte-derived hormone, induces a decrease in food intake and increases energy expenditure via hypothalamic interactions. In animal models obesity can be caused by leptin deficiency or by a dysfunction of the hypothalamic leptin receptor. Using a radioimmunoassay for the determination of leptin in human serum, we measured serum leptin levels in 227 otherwise healthy normal weight (N = 78; body mass index = 16.1–27.7 kg/m2) or obese women (N = 149; body mass index = 27.8–56.7 kg/m2). Fifty-three subjects were followed over a period of 12 weeks under weight reduction (800 kcal/day) and a subgroup of 33 for another 13 weeks after termination of the diet. Body mass index and serum leptin concentrations were measured longitudinally and compared to female controls not under diet. Under baseline conditions, log serum leptin levels were positively related to body mass index with a best fit using a non-linear regression (p < 0.001), indicating an attenuated increase in serum leptin levels with high body mass index. No subgroup with low serum leptin levels could be identified. Weight reduction induced a rapid decrease in serum leptin levels within the first 3 weeks to levels significantly lower than in body mass index-matched controls under normal diet (p < 0.001). This pattern was consistent after 6 and 12 weeks. Serum leptin levels increased again after the end of the diet but remained significantly lower than in the controls despite unrestricted calorie intake over 7 weeks. The rapid and persistent decrease in serum leptin to lower levels than expected from matched controls may explain the pertinent difficulties of obese subjects to cope with weight reduction.
G Brabant, Abt. Klinische Endokrinologie Medizinische Hochschule Hannover, Konstanty-Gutschowstr. 8, D-30623 Hannover, Germany
Free and total insulin-like growth factors and insulin-like growth factor binding proteins during 14 days of growth hormone administration in healthy adults
Authors: Skjæbæk Christian , Frystyk Jan , Møller Jens , Christiansen Jens Sandahl , Ørskov Hans 
Published: December 2008

Skjærbæk C, Frystyk J, Møller J, Christiansen JS, Ørskov H. Free and total insulin-like growth factors and insulin-like growth factor binding proteins during 14 days of growth hormone administration in healthy adults. Eur J Endocrinol 1996;135:672–7. ISSN 0804–4643
The objective was to investigate the effect of growth hormone (GH) administration on circulating levels of free insulin-like growth factors (IGFs) in healthy adults. Eight healthy male subjects were given placebo and two doses of GH (3 and 61U/m2 per day) for 14 days in a double-blind crossover study. Fasting blood samples were obtained every second day. Free IGF-I and IGF-II were determined by ultrafiltration of serum. Total IGF-I and IGF-II were measured after acid–ethanol extraction. In addition, GH, insulin, IGF binding protein 1 (IGFBP-1) and IGFBP-3 were measured. Serum-free and total IGF-I increased in a dose-dependent manner during the 14 days of GH administration. After 14 days, serum-free IGF-I values were 610 ± 100 ng/l (mean±sem) (placebo), 2760 ± 190 ng/l (3IU/m2) and 3720 ± 240 ng/l(6 IU/m2) (p = 0.0001 for 3 and 6 IU/m2 vs placebo; p = 0.004 for 3 IU/m2 vs 6 IU/m2). Total IGF-I values were 190 ± 10 μg/l (placebo), 525 ± 10 (3 IU/m2), and 655 ± 40 μg/l (6 IU/m2) (p < 0.0001 for 3 and 6IU/m2 vs placebo; p = 0.04 for 3 IU/m2 vs 6 IU/m2). There were no differences in the levels of free or total IGF-II during the three study periods. Insulin-like growth factor binding protein 1 was decreased during GH administration (p = 0.04 for placebo vs 3IU/m2; p = 0.006 for placebo vs 6 IU/m2). In conclusion, fasting serum free IGF-I increased dose dependently during GH administration and free IGF-I increased relatively more than total IGF-I. This may partly be due to the decrease in IGFBP-1.
Christian Skjærbæk, Institute of Experimental Clinical Research, Medical Research Laboratories, Aarhus Kommune Hospital, Norrebrogade 44, DK-8000 Aarhus C, Denmark
High plasma levels of endothelin-1 in untreated Addison's disease
Authors: Letizia Claudio , Centanni Marco , Scuro Luigi , Canettieri Gianluca , Cerci Sabrina , De Ciocchis Anita , D'Ambrosio Cecilia , Scavo Domenico 
Published: December 2008

Letizia C, Centanni M, Scuro L, Canettieri G, Cerci S, De Ciocchis A, D'Ambrosio C, Scavo D. High plasma levels of endothelin 1 in untreated Addison's disease. Eur J Endocrinol 1996;135:696–9. ISSN 0804–4643
The aim of this study has been to investigate the plasma endothelin-1 (ET-1) levels in adult patients with proven Addison's disease (AD). Plasma ET-1 levels were measured in 29 subjects (17 males and 12 females, aged between 20 and 54 years): 15 of them were patients with AD and 14 were sex- and age-matched normal subjects, used as a control group. All patients with AD have been studied under basal conditions and nine of them also after 2 weeks on oral corticosteroid therapy (individual cortisol dosage ranging from 25 to 37.5 mg/day and 0.1 mg/day 9α-fluorohydrocortisone). Extracted plasma ET-1 was determined by a specific radioimmunoassay using rabbit endothelin antisera. Mean ET-1 values in the patients with AD were three times higher than in normal subjects (21.09 ± 4.38 pg/ml vs 6.72 ± 1.74 pg/ml; p < 0.0001). Plasma ET-1 levels assayed in the patients with AD after 2 weeks of corticosteroid therapy were significantly decreased (14.47 ± 3.7 pg/ml vs 22.8 ± 5.2 pg/ml; −37%; p < 0.001) compared to values in untreated patients. However, the plasma ET-1 values obtained following corticosteroid therapy were still significantly higher (p < 0.001) than those detected in the control subjects. These results clearly indicate that patients with untreated AD have increased circulating ET-1 levels that may be reduced by short-term corticosteroid therapy.
Claudio Letizia, Policlinico Umberto I, II Clinica Medica, 00185 Roma, Italy
Effects of UK-14,304, noradrenaline, and propranolol on insulin release from transplanted mouse islets
Authors: Shi Chun-Liang , Sehlin Janove , Täljedal Inge-Bert 
Published: December 2008

Shi C-L, Sehlin J, Täljedal, I-B. Effects of UK-14,304, noradrenaline, and propranolol on insulin release from transplanted mouse islets. Eur J Endocrinol 1996;135:724–8. ISSN 0804-4643
To elucidate the adrenergic responsiveness of transplanted pancreatic islets, normal BALB/c mice received 150 syngeneic islets under the left kidney capsule. After 12–40 weeks, the grafts were removed and compared with untransplanted islets by an in vitro perifusion technique. Noradrenaline (NA), 3 μmol/l, completely inhibited glucose-stimulated insulin release from untransplanted islets but not from grafts, whether or not the β adrenergic blocker, L-propranolol, was present. UK-14,304, an α2-specific adrenergic agonist, inhibited glucose-induced insulin secretion from untransplanted islets by 80–92% at 0.1 or 1 μmol/l, and by 35–56% at 5–10 nmol/l, Insulin secretion from islet grafts was also markedly inhibited by 0.1 or 1 μmol/l, but not by 5 or 10 nmol/l, UK-14,304. It is suggested that the diminished adrenergic inhibition of insulin release from islet grafts reflects an altered function of the α2 adrenoceptors on the β-cells.
Chun-Liang Shi, Department of Histology and Cell Biology, Umeå University, S-901 87 Umeå, Sweden
Proinflammatory cytokines interleukin 1β and tumor necrosis factor α inhibit growth hormone stimulation of insulin-like growth factor I synthesis and growth hormone receptor mRNA levels in cultured rat liver cells
Authors: Wolf Matthias , Böhm Sebastian , Brand Marcus , Kreymann Georg 
Published: December 2008

Wolf M, Böhm S, Brand M, Kreymann G. Proinflammatory cytokines interleukin 1β and tumor necrosis factor α inhibit growth hormone stimulation of insulin-like growth factor I synthesis and growth hormone receptor mRNA levels in cultured rat liver cells. Eur J Endocrinol 1996;135:729–37. ISSN 0804–4643
Low levels of insulin-like growth factor I (IGF-I) in critical illness are observed despite increased or normal levels of growth hormone (GH). The mechanisms for this apparent GH resistance have not been elucidated. As many of the acute inflammatory responses in critical illness are mediated by the proinflammatory cytokines interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α), the present studies evaluated IL-1β and TNF-α effects on steady-state and GH-stimulated IGF-I synthesis and GH receptor mRNA levels. In rat hepatocytes in primary culture, IGF-I released into culture medium was determined by radioimmunoassay, and quantitative competitive polymerase chain reaction was used to measure IGF-I mRNA and GH receptor mRNA concentrations. Growth hormone increased GH receptor mRNA, IGF-I mRNA and IGF-I protein secreted into the culture medium. In cells not stimulated with GH, modest inhibitory effects of IL-1β on GH receptor mRNA, IGF-I mRNA and IGF-I protein levels were seen. However, the stimulatory effects of GH were inhibited in a dose-dependent manner both by IL-1β and TNF-α, and at higher cytokine concentrations no stimulatory effects of GH were observed. Both IL-1β and TNF-α in submaximal dose had additive inhibitory effects on IGF-I protein concentrations but these effects did not result in irreversible damage to cells, as indicated by restoration of IGF-I and GH receptor mRNA levels to normal after withdrawal of cytokines. In conclusion, we demonstrated that in rat hepatocytes in primary culture IL-1β and TNF-α inhibited GH-stimulated IGF-I synthesis. Diminished GH receptor mRNA concentrations in response to IL-1β and TNF-α indicate that low IGF-I levels during severe illness, despite high circulating GH levels, may at least partially be a consequence of suppression of hepatic GH receptor synthesis by IL-1β and TNF-α.
Matthias Wolf, Medizinische Kern- und Poliklinik, Universitäts-Krankenhaus Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany
Effect of vitamin D treatment in hypoparathyroid patients: a study on calcium, phosphate and magnesium homeostasis
Authors: Mortensen Lene , Hyldstrup Lars , Charles Peder 
Published: December 2008

Abstract
Aim: This study was undertaken to examine the effects of long-term vitamin D treatment on calcium, phosphate and magnesium homeostasis at organ level in hypoparathyroid patients.
Methods: Fifteen vitamin D-treated hypoparathyroid patients were studied, eight of the patients in a combined 47Ca kinetic and calcium, phosphate and magnesium balance study. Results were compared with a matched control group of 12 normal individuals.
Results: All the patients had normal serum levels of calcium, phosphate and magnesium. Absolute intestinal calcium absorption was increased (P <00001). Urinary calcium excretion was normal, but active tubular calcium reabsorption (TmCa/glomerular filtration rate) was low (P<0·001). Bone resorption rates and bone mineralization rates were very low (P <0001 and P <0·05). Twenty-four-hour urinary hydroxyproline excretion and serum cross-linked carboxyterminal telopeptide of type I were in the upper normal range. Serum alkaline phosphatase was normal, but serum carboxyterminal propeptide of human type I procollagen and serum osteocalcin were significantly reduced (P <0·05). Calcium balance was positive and significantly different from controls (P <0·001). All parameters from phosphate homeostasis were normal. Intestinal magnesium absorption was low though not significantly different from normal (P = 0·06). Urinary excretion of magnesium was not significantly higher than normal, but renal magnesium reabsorption was reduced (P <0·001). Magnesium balance was low, though the difference was not significant (P <0·06).
Conclusion: Long-term vitamin D treatment in hypoparathyroid patients resulted in a positive calcium balance. Bone turnover was very low. Results of bone markers and resorption rate were conflicting. Vitamin D treatment apparently normalized the abnormalities previously found in phosphate homeostasis of hypoparathyroid patients. Magnesium homeostasis was disturbed, with a more negative balance compared with normal subjects, implying a state of magnesium deficiency in these patients.
European Journal of Endocrinology 136 52–60
Lipoprotein(a) increase associated with thyroid autoimmunity
Authors: Lotz Helga , Salabè Giovanni B 
Published: December 2008

Abstract
Conflicting results have been reported regarding serum lipoprotein(a) (Lp(a)) concentrations in patients with hypothyroidism. We addressed the question whether thyroid autoimmunity could be associated with elevated Lp(a) values independent of the thyroid status. Lp(a) was measured by ELISA in 30 males, 29 premenopausal and 30 postmenopausal females positive for thyroid peroxidase- and/or thyroglobulin-antibody (T-Abs) and normolipidemic, screened out respectively from 428 male donors, 162 premenopausal donors and 108 postmenopausal females; they were compared with 65 males, 72 premenopausal and 48 postmenopausal females, negative for thyroid antibodies, normolipidemic and matched for age. T-Abs-positive male donors showed serum Lp(a) concentrations significantly increased compared with males without T-Abs (mean 19·7 ± 15·9 vs 12·7 ± 17·5 mg/dl; median 17·0 vs 4·0 mg/dl; Mann Whitney U test: P = 0·0000). In premenopausal females no difference could be found between T-Abs-positive and T-Abs-negative subjects (mean 13·2 ± 16·1 vs 12·3 ± 13·9 mg/dl; median 5·2 vs 8·7 mg/dl), suggesting an Lp(a) lowering effect of estrogens. The study was, therefore, extended to postmenopausal females. Significantly elevated Lp(a) levels were found in 30 postmenopausal females with T-Abs when compared with 48 postmenopausal females without T-Abs (40·0 ± 34·2 mg/dl vs 20·7 ± 19·3 mg/dl; median 32·0 vs 18·0 mg/dl; Mann Whitney U test: P = 0·0002). Finally, 21 postmenopausal, normolipidemic, autoimmune hypothyroid patients on l-thyroxine and euthyroid compared with 48 postmenopausal females without T-Abs also showed increased serum levels of Lp(a) (mean 27·0 ± 16·8 mg/dl vs 20·7 ± 19·3 mg/dl, median 25·0 vs 18 mg/dl; Mann Whitney U test: P = 0·0024). Thyrotropin levels in all subjects and patients were within the normal range. In conclusion, our results in males and postmenopausal females with T-Abs and euthyroid show an association between thyroid autoimmunity and increased levels of Lp(a), while the results obtained in premenopausal females suggest that estrogens might interfere with the Lp(a) increase related to thyroid autoimmunity.
European Journal of Endocrinology 136 87–91
Biologically active human islet amyloid polypeptide/amylin in transgenic mice
Authors: van Hulst Karen L , Born Walter , Muff Roman , Oosterwijk Cor , Blankenstein Marinus A , Lips Cornelis JM , Fischer Jan A , Höppener Jo WM 
Published: December 2008

Abstract
Objective: Human islet amyloid polypeptide (hIAPP), also named amylin, is a pancreatic β cell protein implicated in the pathogenesis of pancreatic islet amyloid formation and type 2 diabetes mellitus. To study the (patho)physiological roles of hIAPP, we have generated transgenic mice that overexpress hIAPP mRNA, in relation to endogenous mouse IAPP (mIAPP) mRNA, in pancreatic β cells. The biological activity of human and mouse IAPP derived from pancreatic extracts was determined.
Methods: Pancreatic and plasma extracts of transgenic and control mice were analyzed by reversedphase high-performance liquid chromatography (HPLC) and radioimmunoassay, yielding a separation of hIAPP from mIAPP. Biological activity of immunoreactive human and mouse IAPP components derived from pancreatic extracts was assessed by calcitonin receptor-mediated stimulation of cyclic AMP accumulation in T47D human breast carcinoma cells.
Results: The predominant immunoreactive human and mouse IAPP gene products had the retention times on HPLC analysis of the corresponding synthetic peptides. The ratio of bioactive over immunoreactive hIAPP and mIAPP was 0·93 ±0·18 and 1·19 ±0·56 respectively. In extracts of two plasma pools from 4 transgenic animals, hIAPP was 4·6- to 7-fold more abundant than mIAPP.
Conclusion; This study has shown that correctly processed hIAPP produced in transgenic mouse pancreatic β cells exhibits full biological activity. The results validate these transgenic mice for the study of (patho)physiological roles of hIAPP in vivo.
European Journal of Endocrinology 136 107–113
Abnormal carotid arterial wall dynamics in symptom-free hypopituitary adults
Authors: Markussis Viron , Beshyah Salem A , Fisher Charles , Parker Kim H , Nicolaides Andrew N , Johnston Desmond G 
Published: December 2008

Abstract
Objective: Although vascular mortality is increased in hypopituitary adults on routine replacement, there are limited data on the atherosclerotic process during life in these patients. Measurement of arterial stiffness may provide an index of early vascular changes that predispose to the development of major vascular accidents.
Design: Thirty-four hypopituitary adults on conventional replacement therapy and 39 age- and sex-matched controls were studied. They had no history or clinical evidence of macrovascular disease. The common carotid artery distensibility coefficient (DC), compliance coefficient (CC) and arterial stiffness index (beta index) were calculated from high-resolution ultrasonic imaging of the two common carotid arteries and from the brachial blood pressure.
Results: There was no difference between patients and controls in carotid diastolic diameter (mean ± s.e.m.) (5·55 ± 0·16 vs 5·45 ± 0·08 mm) and pulse pressure (6·66 ± 0·30 vs 6·58 ± 0·24 kPa). The increase in diameter during systole was significantly lower in the hypopituitary patients (0·39 ± 0·02 vs 0·50 ±0·03 mm, P < 0·001). The DC was significantly lower in patients than in controls (24·2 ± 2·29 vs 30·1 ± 2·01 10−3kPa−1, P < 0·05). The carotid CC was also significantly lower in patients than in controls (5·7 ± 0·49 vs 7·0 ± 0·45 10−7m2kPa−1, P < 0·05). The beta index was higher in the patient group (8·4 ± 1·3 vs 5·9 ± 0·37, P < 0·05). When men and women were considered separately, the differences between patients and controls were statistically significant in women but not in men and were more marked in the older women subgroup.
Conclusions: Asymptomatic hypopituitary adults (especially women) on conventional replacement therapy have increased stiffness of the common carotid arteries. These findings provide additional evidence for a process leading to premature atherosclerosis in this group of patients.
European Journal of Endocrinology 136 157–164
Population-based reference values for IGF-I and IGF-binding protein-1: relations with metabolic and anthropometric variables
Authors: Nyström Fredrik H , Öhman Peter K , Ekman Bertil Å , Österlund Maria K , Karlberg Bengt E , Arnqvist Hans J 
Published: December 2008

Abstract
Population-based reference values for IGF-I and IGF-binding protein-1 (IGFBP-1) have been established. One hundred and one women and the same number of men, 20–70 years old, were randomly selected from the population registry in the community of Linköping. Participation rate was 67%. Venous blood was drawn in the fasting state. Serum IGF-I was measured by RIA after acid-ethanol extraction and IGFBP-1 was determined by ELISA. IGF-I levels did not differ between genders and the decline with age was similar in men and women (men: Y=366–3·28×age (years), r =−0·61, P<0·0001; women: Y=386–3·49×age, r =−0·57, P<0·0001, P=0·4 for difference in slope). There were negative correlations between IGF-I and plasma lipids and blood pressure in both genders, but none was independent of age. Serum angiotensin-converting enzyme activity correlated positively with IGF-I in men independently from age (r =0·21, P=0·01). The distribution of IGFBP-1 was positively skewed and it was higher in women than in men (5·9±4·8 μg/l and 4·0±3·3 μg/l respectively; Mann–Whitney, P=0·002). In men and in the women not taking oestrogen, IGFBP-1 correlated positively with age (Spearman rank correlation (Spearman): men: r=0·32, P=0·002; women: r=0·24, P=0·03). C-peptide correlated negatively (Spearman: men: r =−0·38, P=0·002; women: r =−0·49, P<0·000) and sex hormone binding globulin positively with IGFBP-1 (Spearman: men: r=0·50, P<0·0001; women: r =0·55, P<0·0001).
IGF-I declined with age while IGFBP-1, which is considered to modulate the free bioactive fraction of IGF-I, increased. This suggests that IGF-I activity might be even lower in elderly subjects than is accounted for by the low total IGF-I.
European Journal of Endocrinology 136 165–172
Increased circulating leptin concentrations in insulin-resistant first-degree relatives of patients with non-insulin-dependent diabetes mellitus: relationship to body composition and insulin sensitivity but not to family history of non-insulin-dependent diabetes mellitus
Authors: Nyholm Birgit , Fisker Sanne , Lund Sten , Møller Niels , Schmitz Ole 
Published: December 2008

Abstract
Objective: To explore a possible association between serum concentration of leptin, insulin sensitivity and non-insulin-dependent diabetes mellitus (NIDDM).
Design: Forty first-degree relatives of NIDDM patients and 35 control subjects matched for age, gender and body mass index underwent a hyperinsulinaemic (insulin infusion rate 0·6 mU/kg per min) euglycaemic clamp combined with indirect calorimetry. Serum leptin was measured in fasting blood samples obtained before the clamp.
Results: All subjects had a normal oral glucose tolerance test. Insulin-stimulated glucose uptake (M) was decreased in the relatives compared with the control subjects (4·58 ± 0·27 versus 606 ± 0·25 mg/kg per min, P < 0·001). Conversely, serum leptin was increased in the relatives (9·6·/÷ 1·1 versus 6·1·/÷ 1·2 ng/ml (geometric mean·/÷ antilog s.e.m.). P < 0·05). A positive correlation was observed between circulating levels of leptin and percentage body fat (P < 0·001) and inverse correlations were found between leptin, M (P < 0·01), maximal aerobic capacity (VO2 max) (P < 0·01), and energy expenditure (P ≤ 0·01) in both groups. In multiple linear regression analysis, percentage body fat, gender and M significantly determined the level of leptin (r2 = 0·71, P < 0·001) whereas family history of NIDDM and VO2 max did not.
Conclusion: Serum leptin is increased in insulin-resistant offspring of NIDDM patients. The association between leptin, anthropometric measures and insulin sensitivity is, however, comparable with that of a control group. The increased concentrations of serum leptin in the relatives appear to be associated with the insulin resistance, but not with a family history of NIDDM.
European Journal of Endocrinology 136 173–179