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  • 1
    Digitale Medien
    Digitale Medien
    The binding of insulin to mouse leucocytes during viral infections (1983)
    Springer
    Diabetologia 25 (1983), S. 521-524 
    Details
    ISSN: 1432-0428
    Schlagwort(e): Insulin binding ; viral infections ; encephalomyocarditis virus ; herpes simplex virus ; lactic dehydrogenase virus ; bacterial lipopolysaccharide ; murine splenic leucocytes ; liver membranes
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The effect of viral infections on insulin binding in vivo was evaluated by measuring the binding of 125I-insulin to several different tissues. We found that splenic leucocytes from mice infected with either the diabetogenic (D) or non-diabetogenic (B) variants of encephalomyocarditis virus, herpes simplex virus, or lactic dehydrogenase virus showed up to a 130% increase in insulin binding. As much as a 300% increase in the binding of 125I-insulin to splenic leucocytes was observed in mice given bacterial lipopolysaccharide. In neither virus-infected nor lipopolysaccharide-treated mice was there any substantial change in insulin receptors on thymocytes, liver membranes, or peripheral erythrocytes. Thus, the increased binding of insulin appears to be limited to leucocytes and does not appear to represent a generalized metabolic alteration. These experiments suggest that during infection, the binding of insulin to leucocytes, which is widely used to measure insulin receptors, may not always accurately reflect the insulin receptor status of other tissues.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00284463
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  • 2
    Digitale Medien
    Digitale Medien
    In vivo imaging and quantitative analysis of insulin-receptor interaction in lean and obese Zucker rats (1984)
    Springer
    Diabetologia 26 (1984), S. 229-233 
    Details
    ISSN: 1432-0428
    Schlagwort(e): 123I-Insulin ; Zucker rats ; receptors ; scintillation scanning ; computer analysis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Imaging and quantitative analysis of insulin-receptor interaction was studied in vivo in lean and obese Zucker rats, using a recently developed technique in which purified Tyr A14 123I-monoiodoinsulin is intravenously injected and the tracer followed by scintillation scanning. The obese rats were 72% overweight, had near normal blood glucose concentrations and an 11-fold increase in plasma insulin concentration. In both groups of rats, the tracer was rapidly taken up by the liver (by a receptor mediated mechanism) and the kidneys (by a non-receptor mediated process). Past this maximum, radioactivity decreased in both organs as 123I-insulin was degraded and free 123I-iodide was released into the plasma compartment. Heart radioactivity (i.e. blood pool) mirrored that of the liver and kidneys. The rapid initial decrease of blood radioactivity was concomitant with liver and kidney uptake of 123I-insulin. Release of free iodide from these organs induced a slow secondary rise of blood radioactivity followed by a final decline corresponding to clearance of plasma iodide, mainly by urinary excretion. Liver radioactivity profiles of lean and obese rats were parallel. When expressed per g weight, liver radioactivity was significantly decreased in obese rats. However, due to hepatomegaly in obese rats, total liver radioactivity was significantly higher in homozygous fa/fa rats than in lean littermates. Furthermore, if the marked hyperinsulinaemia of the obese rats is taken into account, total bound insulin was enhanced in the liver of fa/fa rats whatever reference is used, either g weight or total liver. The kidney profile of radioactivity of both rats was not significantly different. In conclusion: (1) obese rats are insulin resistant as near normal glycaemia is achieved at the price of a marked hyperinsulinaemia; (2) liver uptake of insulin is enhanced in obese rats, and (3) the insulin resistance syndrome of fa/fa rats is not due to a decrease in liver insulin receptor number and/or affinity but rather to as yet unknown event(s) subsequent to receptor binding.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00252413
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  • 3
    Digitale Medien
    Digitale Medien
    Activation of liver and muscle insulin receptor tyrosine kinase activity during in vivo insulin administration in rats (1990)
    Springer
    Diabetologia 33 (1990), S. 77-83 
    Details
    ISSN: 1432-0428
    Schlagwort(e): Hyperinsulinaemic glucose clamp ; skeletal muscle ; liver ; insulin receptors ; tyrosine kinase ; insulin resistance ; β-subunit C-terminus
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary We have studied autophosphorylation and tyrosine kinase activity of the insulin receptor purified from liver and muscle of fasted rats before and after infusion of insulin (100 mU/h) during a 2.5 h glucose clamp. Recovery of insulin receptors and insulin binding to the solubilised receptors was unaffected by the glucose clamp. Autophosphorylation of the insulin receptor β subunit was increased in liver receptors prepared from rats at the end of the glucose clamp compared to rats in the basal state both in the absence of insulin in vitro (109% increase, p〈0.001) and after in vitro stimulation with 10−7 mol/l insulin (clamped vs fasted; 96% increase, p〈0.001). Insulin (10−7 mol/l) stimulated autophosphorylation was also increased in muscle receptor preparations from clamped rats compared with rats in the basal state (58% increase, p〈0.05). In both liver and muscle receptors, the clamp increased the amount of [32P]-phosphate incorporated into the β subunit without changing the sensitivity of the insulin stimulation. HPLC analysis of the tryptic phosphopeptides derived from the β subunit after insulin stimulated autophosphorylation of liver receptors revealed an increase of 32P in all phosphorylation sites without any change in the overall pattern. Tyrosine kinase activity of liver and muscle insulin receptors from clamped rats was also increased approximately twofold (p〈0.05) when analysed using a synthetic substrate (poly Glu4 Tyr1). Our results support the notion that the insulin receptor exists in an active and inactive form, and that elevated plasma insulin concentrations increases the proportion of active receptors.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00401044
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  • 4
    Digitale Medien
    Digitale Medien
    Anti-insulin receptor antibodies inhibit insulin binding and stimulate glucose metabolism in skeletal muscle (1978)
    Springer
    Diabetologia 14 (1978), S. 311-317 
    Details
    ISSN: 1432-0428
    Schlagwort(e): Anti-insulin receptor antibodies ; insulin-like effects ; insulin resistance ; skeletal muscle ; insulin receptor ; insulin binding ; insulin action ; glucose transport ; glycolysis ; glycogen synthesis ; obese mice
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Autoantibodies against the insulin receptor are found in the serum of some patients with severe insulin resistance. The effects of one of these sera on insulin binding and on glucose transport and metabolism were investigated in the isolated mouse soleus muscle. Preincubation of muscles with the patient's serum resulted in an inhibition of subsequent125I-insulin binding (half-maximal effect at 1∶500 dilution) and in a two to three-fold stimulation of glucose transport and metabolism (half-maximal effect at 1∶2000 dilution). The insulin-like effects were blocked by anti-human IgG, but not by antiinsulin antibodies. The magnitude of the serum effects on 2-deoxyglucose uptake and glycolysis was similar to that of insulin, but the effect on glycogen synthesis was smaller than that of insulin. It is suggested that the patient's serum and insulin promote glucose transport and glycolysis through a common pathway, but act differently on glycogen synthesis.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF01223022
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