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  • 1
    Electronic Resource
    Electronic Resource
    The binding of insulin to mouse leucocytes during viral infections (1983)
    Springer
    Diabetologia 25 (1983), S. 521-524 
    Details
    ISSN: 1432-0428
    Keywords: Insulin binding ; viral infections ; encephalomyocarditis virus ; herpes simplex virus ; lactic dehydrogenase virus ; bacterial lipopolysaccharide ; murine splenic leucocytes ; liver membranes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00284463
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    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
    Keywords: Hyperinsulinaemic glucose clamp ; skeletal muscle ; liver ; insulin receptors ; tyrosine kinase ; insulin resistance ; β-subunit C-terminus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401044
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    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
    Keywords: Anti-insulin receptor antibodies ; insulin-like effects ; insulin resistance ; skeletal muscle ; insulin receptor ; insulin binding ; insulin action ; glucose transport ; glycolysis ; glycogen synthesis ; obese mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01223022
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Insulin binding and activation of glycogen synthase in fibroblasts from type 1 (insulin-dependent) diabetic patients (1982)
    Springer
    Diabetologia 23 (1982), S. 431-435 
    Details
    ISSN: 1432-0428
    Keywords: Human fibroblasts ; insulin receptors ; glycogen synthase ; Type 1 diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 125I-Insulin binding and insulin stimulation of glycogen synthase were examined in fibroblasts cultured from nine Type 1 (insulin-dependent) diabetic patients with age of onset of 〈42 years. In all cases specific insulin binding was qualitatively and quantitatively normal. Total 125I-insulin binding was elevated in cells from three patients with early onset diabetes (two with onset before age 1 year) due to an increase in ‘non-specific’ binding. When the ability of insulin to stimulate the conversion of the glucose-6-phosphate dependent to the glucose-6-phosphate independent form of glycogen synthase was measured, all cell lines responded, albeit to differing degrees. In general, the response of cells from diabetic donors was more variable than that of control fibroblasts. A slightly lower level of cellular glycogen was evident in the cells of the diabetic patients, and this was mirrored in slightly higher levels of the independent form of the enzyme. The average maximal level of the independent form of the enzyme also was higher in the diabetic patients' cells. Fibroblasts from one of the patients with very early onset diabetes had glycogen synthase levels that were markedly lower than in any other cell line examined. In summary, fibroblasts cultured from Type 1 diabetic patients do not show major defects in either insulin binding or action. A suggestion of subtle differences in the cells from the diabetic patients, particularly those with very early onset, is evident, however. Whether these are secondary to some primary genetic defect or represent some selection during culture remains to be determined.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00260957
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    Paper (German National Licenses)
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