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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 113 (1964), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Physics Letters A 58 (1976), S. 102-104 
    ISSN: 0375-9601
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Chemical Physics Letters 58 (1978), S. 87-90 
    ISSN: 0009-2614
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1440
    Keywords: CIAA ; CF-ICA ; Beta-cell function ; IVGTT ; HLA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Out of a random population of 4208 non-diabetic pupils without a family history of Type I diabetes 44 (1.05%) individuals had islet cell antibody (ICA) levels greater or equal to 5 Juvenile Diabetes Foundation (JDF) units. 39 of these ICA-positives could be repeatedly tested for circulating insulin autoantibodies (CIAA) using a competitive radiobinding assay. The results were compared with the insulin responses in the intravenous glucose tolerance tests (IVGTT) and with HLA types. Six pupils were positive for CIAA. All of them had complement-fixing ICA, and 5 of them were HLA-DR4 positive. Three of the 6 showed a first-phase insulin response below the first percentile of normal controls. Our data indicate that in population-based studies CIAA can be considered as a high risk marker for impaired beta-cell function in non-diabetic ICA-positive individuals.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1433-0474
    Keywords: Schlüsselwörter Ullrich-Turner-Syndrom ; STH-Mangel ; Insulinresistenz ; Hyperinsulinismus ; Gestörte Glukosetoleranz ; Key words Ullrich-Turner-syndrome ; GH deficiency ; Insulin resistance ; Hyperinsulinism ; Impaired glucose tolerance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Background: An increased incidence of diabetes mellitus in patients with hypersecretion of growth hormone (acromegaly, pituitary gigantism) is well known. In the present study, the effect of long-term growth hormone (GH) therapy on basal as well as stimulated blood glucose and insulin concentrations was studied in pediatric patients. Methods: During an oral glucose tolerance test, plasma glucose and insulin were measured every 30 minutes. 2 groups of patients were studied before and during GH therapy: 9 patients with complete or partial GH deficiency (mean age at initiation of therapy: 9.1 ± 1.0 years) as well as 11 girls with Turner syndrome (mean age: 10.8 ± 0.9 years). Results: A weekly dose of growth hormone of 12.8 ± 0.9 units/m2 did not increase blood glucose in patients with GH deficiency, all patients displayed normal glucose tolerance. In contrast, the integrated secretion of insulin during the OGT-test increased from 3.7 ± 0.8 U/l × min before therapy to 5.9 ± 0.6 after 1 year (p 〈 0.005; Wilcoxon). Hyperinsulinism was still present after 2 years of GH therapy (n = 7). In Ullrich-Turner patients, a significantly higher dose of growth hormone was used (mean: 22.4 ± 2.0 Units/m2× week). After 1 year of GH therapy, blood glucose 30 min after the ingestion of oral glucose had increased to 167 ± 6 mg/dl compared to 147 ± 7 mg/dl before GH administration (p = 0.05). One girl developed impaired glucose tolerance. Insulin secretion rose by more than 100 % (AUC for insulin before therapy: 4.1 ± 0.3 U/l × min, after 1 year of therapy: 9.5 ± 1.4). In 8 Ullrich-Turner girls, the OGT-test was repeated again after 3 years of GH therapy, insulin secretion continued to be clearly elevated (AUC: 10.8 ± 2.1 U/l × min). Conclusions: GH therapy for 1 year increases insulin release during the OGT-test by 59 % in patients with GH deficiency and by 131 % in Ullrich-Turner syndrome. This difference may be due to a higher dose, or due to a specific tendency for insulin resistance in girls with gonadal dysgenesis. The long-term consequences of hyperinsulinism (hypertension, cardiovascular risk) cannot be predicted in these patients and should be followed in prospective studies.
    Notes: Zusammenfassung Fragestellung: Das gehäufte Auftreten eines Diabetes bei Wachstumshormonüberproduktion (Akromegalie, hypophysärer Gigantismus) ist lange bekannt. Methode: Im oralen Glukosetoleranztest (OGT) wurden Blutzucker und Insulin alle 30 min bestimmt. Zwei Patientengruppen wurden untersucht: 9 Patienten mit komplettem oder partiellem STH-Mangel (Alter bei Therapiebeginn 9,1 ± 1,0 Jahre) sowie 11 Mädchen mit Ullrich-Turner-Syndrom (10,8 ± 0,9 Jahre). Ergebnisse: Bei den STH-Mangelpatienten zeigte sich unter einer wöchentlichen STH-Dosis von 12,8 ± 0,9 E/m2 (Mittelwert ± SEM) kein Anstieg des Blutzuckers, die Glukosetoleranz war stets normal. Dagegen stieg die integrierte Insulinsekretion während des OGT-Tests von 3,7 ± 0,8 U/l und min vor der Therapie auf 5,9 ± 0,6 nach 1 Jahr an (p 〈 0,005; Wilcoxon). Ullrich-Turner-Patientinnen erhielten eine deutlich höhere STH-Dosis (im Mittel 22,4 ± 2,0 E/m2 und Woche). Nach 1 Jahr STH-Therapie zeigte sich ein vermehrter Anstieg des Blutzuckers 30 min nach oraler Glukosegabe (167 ± 6 mg/dl versus 147 ± 7 vor STH-Therapie; p = 0,05), ein Mädchen entwickelte eine gestörte Glukosetoleranz. Die Insulinsekretion stieg auf mehr als das Doppelte an (Integral: 4,1 ± 0,3 U/l und min vor Therapie, 9,5 ± 1,4 nach 1 Jahr STH-Gabe; p 〈 0,001). Schlußfolgerungen: Eine STH-Therapie für 1 Jahr erhöht die Insulinsekretion im OGT-Test um 59 % bei Patienten mit STH-Mangel und um 131 % bei Ullrich-Turner-Syndrom. Langfristige Auswirkungen des Hyperinsulinismus (Hypertonie, kardiovaskuläres Risiko) sollten in prospektiven Studien verfolgt werden.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 32 (1989), S. 198-202 
    ISSN: 1432-0428
    Keywords: Skeletal growth ; somatomedin ; insulin ; growth hormone ; rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of insulin on skeletal growth was examined by (1) systemic injection, (2) local administration into the tibia growth plate and (3) in vitro by use of chondrocytes in culture. (1) Male rats, body weight 60–75 g, were hypophysectomised. One week after the operation, the animals were divided into three groups. Group A received intraperitoneally saline, group B insulin (5–30 U·kg−1·day−1) and group C human growth hormone (250 μg/kg/day) for the following 10 days. In addition, on day 10 the rats were injected with 10 μCi 35-S-sulfate intraperitoneally. Twenty-four h later in the non-fasting state plasma glucose, insulin, somatomedin activity (porcine assay), body weight, nose-rump length, width of the tibia growth plate, and the 35-S-sulfate incorporation into rib cartilage were determined. Compared to saline, growth hormone and insulin treatment significantly enhanced body weights, nose-rumb lengths, the widths of the proximal tibia growth plates and the incorporation of sulfate into rib cartilage. For the three skeletal growth parameters, growth hormone was more effective than insulin, while body weights did not differ after insulin or growth hormone treatment. So matomedin activity (U/ml) was low in group A (0.39±0.04, n=9, Mean±SEM) and group B (0.34±0.08, n=8) and high in the growth hormone treated group C (0.90±0.09, n=7; p〈0.002). (2) To test the possibility that insulin might directly augment skeletal growth, insulin (80 mU) was injected into the proximal tibia growth plate of one leg and saline into the cartilage zone of the other leg. Insulin treatment significantly increased the width of the cartilage zones. Insulin: 211±22 μm, saline 200±22 μm, (Mean±SD, n=6, p〈0.05). (3) Addition of human biosynthetic insulin and growth hormone to the culture medium increased colony formation of chondrocytes in a bell-shaped fashion. A plateau in colony formation was reached with 3.1–6.25 ng/ml insulin and 25–50 ng/ml growth hormone, but with larger dosages of both hormones, the effect was diminished. The results suggest that insulin might stimulate postnatal skeletal growth by a direct effect on the target cells.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: Viral antibodies ; Beta-cell function ; population study
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Viral antibodies were tested in a cohort of 44 isletcell antibody-positive individuals age 7–19 years, and 44 of their islet cell antibody-negative age and sex-matched classmates selected from a population study of 4208 pupils who had been screened for islet cell antibodies. Anti-coxsackie B1-5 IgM responses were detected in 14 of 44 (32%) of the islet cell antibody-positive subjects and in 7 of 44 (16%) control subjects. This difference did not reach the level of statistical significance. None of the islet cell antibody-positive subjects had specific IgM antibodies to mumps, rubella, or cytomegalovirus. There was also no increase in the prevalence or the mean titres of anti-mumps-IgG or IgA and anti-cytomegalovirus-IgG in islet cell antibody-positive subjects compared to control subjects. These results do not suggest any association between islet cell antibodies, and possibly insulitis, with recent mumps, rubella or cytomegalo virus infection. Further studies are required to clarify the relationship between islet cell antibodies and coxsackie B virus infections.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0428
    Keywords: Height ; weight ; obesity ; siblings ; genetic factors ; bone age
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Normal growth and development, as well as the prevention of overweight, are major goals in the treatment of paediatric patients with insulin-dependent diabetes mellitus (IDDM). We therefore evaluated longitudinally the anthropometric measurements of height and weight, as well as bone age, in an unselected group of 389 patients with IDDM treated at one institution. In order to identify genetic influences on these parameters, height and weight were determined in 186 unaffected siblings and 177 pairs of parents. At diagnosis, patients were slightly taller than average (median z score: +0.37). During the subsequent course of diabetes, age-adjusted heights decreased progressively for the first 9 years, catching up again after more than 10 years of diabetes. Bone ages were progressively retarded with increasing duration of diabetes. In 76 patients of 18 years or older, median z-score for height was +0.30, not different from their unaffected siblings (median z-score: +0.22). The correlation with midparental height was identical for diabetic and nondiabetic siblings (r=0.43). In contrast, children with diabetes were significantly heavier (z-score for weight: +0.74 compared to +0.34 in unaffected siblings; p〈0.002). Obesity developed primarily during and after puberty. We conclude that: 1) during the course of diabetes, longitudinal growth is temporarily reduced and maturation is delayed in children with diabetes compared to unaffected siblings. However, this effect of diabetes is transient and small compared to genetic influences on height in an individual child. 2) As a group, children with IDDM become significantly overweight, which is likely to increase the cardiovascular risk during adulthood.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 30 (1987), S. 100-103 
    ISSN: 1432-0428
    Keywords: Fetal rats ; skeletal growth ; streptozotocin ; diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary For largely unknown reasons severe or moderate diabetes of pregnant rats results in pronounced fetal growth retardation. Therefore, some skeletal growth parameters of fetal rats from streptozotocin diabetic mothers were studied in vivo and in vitro. Two days post conception rats were intravenously injected with 65 mg/kg body weight streptozotocin. On day 20 post conception 8 normal and 8 diabetic rat mothers received 5 μCi 3-H thymidine intraperitoneally. One day later the experiments were terminated. Fetal body weight and body length were significantly (p〈0.05–0.001) reduced in the hyperglycaemic rats compared to normal rats, as was the thymidine incorporation into rib cartilage (p〈0.02). In the cell culture colony formation from isolated chondrocytes of normal and hyperglycaemic fetuses was determined. Proinsulin, insulin (62.5–250 ng/ml), insulin-like growth factor I and II (6.25–25 ng/ml) significantly (p〈0.05–0.001) augmented colony formation in a dose-dependent manner, with the somatomedins being 8 times more effective than proinsulin or insulin. Isolated chondrocytes from hyperglycaemic compared to normal fetuses formed significantly (p〈0.05–0.001) fewer colonies in the basal state and in response to all 4 hormones. The results confirm the growth retardation of fetuses from diabetic rat mothers. A reduced responsiveness of chondrocytes from hyperglycaemic fetuses to various growth factors could be demonstrated as compared to cells from normal fetuses.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0428
    Keywords: Key words Height ; weight ; obesity ; siblings ; genetic factors ; bone age.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Normal growth and development, as well as the prevention of overweight, are major goals in the treatment of paediatric patients with insulin-dependent diabetes mellitus (IDDM). We therefore evaluated longitudinally the anthropometric measurements of height and weight, as well as bone age, in an unselected group of 389 patients with IDDM treated at one institution. In order to identify genetic influences on these parameters, height and weight were determined in 186 unaffected siblings and 177 pairs of parents. At diagnosis, patients were slightly taller than average (median z score: + 0.37). During the subsequent course of diabetes, age-adjusted heights decreased progressively for the first 9 years, catching up again after more than 10 years of diabetes. Bone ages were progressively retarded with increasing duration of diabetes. In 76 patients of 18 years or older, median z-score for height was + 0.30, not different from their unaffected siblings (median z-score: + 0.22). The correlation with mid-parental height was identical for diabetic and non-diabetic siblings (r = 0.43). In contrast, children with diabetes were significantly heavier (z-score for weight: + 0.74 compared to + 0.34 in unaffected siblings; p 〈 0.002). Obesity developed primarily during and after puberty. We conclude that: 1) during the course of diabetes, longitudinal growth is temporarily reduced and maturation is delayed in children with diabetes compared to unaffected siblings. However, this effect of diabetes is transient and small compared to genetic influences on height in an individual child. 2) As a group, children with IDDM become significantly overweight, which is likely to increase the cardiovascular risk during adulthood [Diabetologia (1994) 37: 925–929].
    Type of Medium: Electronic Resource
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