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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
    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
    Keywords: 123I-Insulin ; Zucker rats ; receptors ; scintillation scanning ; computer analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00252413
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    Paper (German National Licenses)
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  • 3
    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
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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