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  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 83 (1988), S. 647-654 
    ISSN: 1435-1803
    Keywords: neonatal ratcardiocytes ; IGF ; insulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the newborn several situations of hyperinsulinism can be associated with myocardial hypertrophy and increased contractility. Insulin and the insulin-like growth factors (IGF) are derived from a common ancestral molecule. Insulin exerts mainly metabolic action, whereas the IGFs promote cell multiplication and differentiation. Using an assay system of cultured neonatal myocardial cells the stimulatory action of insulin and the insulin-like growth factors I and II on myocardial cell contractility was investigated. Spontaneously beating aggregates of myocardial cells were synchronized by an electric impulse generator. Contractility was measured via the amplitude of contraction by an optoelectronic system. Insulin at a concentration of 6,250 and 12,500 μU/ml increased the contractility by 11 and 18%; IGF-I at a concentration of 12 and 25 ng/ml, and IGF-II at a concentration of 25 and 50 ng/ml increased the contractility by 16 and 22%, and 13 and 18%, respectively. Lower concentrations did not provoke a significant increase in contractility. Insulin only in supraphysiological doses increases the contractility of neonatal myocardial rat cells, whereas both insulin-like growth factors act in physiological concentrations. Therefore, during hyperinsulinism insulin may increase myocardial contractility via the IGF receptor and not via the insulin receptor.
    Type of Medium: Electronic Resource
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