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  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    Characterization of insulin receptors in patients with the syndromes of insulin resistance and acanthosis nigricans (1980)
    Springer
    Diabetologia 18 (1980), S. 209-216 
    Details
    ISSN: 1432-0428
    Keywords: Insulin receptors ; acanthosis nigricans ; insulin resistance ; insulin receptor autoantibodies ; Type A patients ; Type B patients ; negative cooperativity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This report analyzes the in vitro characteristics of 125I-insulin binding to the monocytes of nine patients with the syndromes of acanthosis nigricans and insulin resistance. The 3 Type A patients (without demonstrable autoantibodies to the insulin receptor) had decreased binding of insulin due to a decreased concentration of receptors. In these patients the residual receptors demonstrated normal dissociation kinetics, negative cooperativity, and were blocked by anti-receptor antibodies in a manner similar to normal cells. In contrast, monocytes from the 6 Type B patients (with circulating anti-receptor autoantibodies) had decreased binding of insulin due to a decrease in receptor affinity. Insulin binding to monocytes of Type B patients demonstrated accelerated rates of dissociation with no evidence of cooperative interactions among insulin receptors. When coupled with previous data, the present studies further suggest that different mechanisms account for the defects in insulin binding and insulin resistance observed in these patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00251918
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    Paper (German National Licenses)
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  • 3
    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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  • 4
    Electronic Resource
    Electronic Resource
    Subpopulations of antibodies directed against evolutionarily conserved regions of the insulin molecule in insulin-treated patients (1982)
    Springer
    Diabetologia 23 (1982), S. 488-493 
    Details
    ISSN: 1432-0428
    Keywords: Insulin antibodies ; insulin structure ; evolution
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the present study, we attempted to define possible subpopulations of antibodies which theoretically could be directed against evolutionarily conserved regions of the insulin molecule in sera from insulin-treated diabetic patients using a variety of labelled and unlabelled insulins which differ widely in structure but are very similar in functional properties. Ten high titre human insulin antisera from patients treated with mixed beef-pork insulin were examined. All sera were found to bind 125I-pork insulin better than labelled chicken insulin which bound better than labelled fish insulin. Detailed studies were conducted with four of the antisera using the pork and fish tracers. With two of the antisera, a subpopulation of antibody could be detected with 125I-fish insulin which had similar affinity for both fish and pork insulin, but reacted much less well with guinea pig insulin and the desoctapeptide derivative of porcine insulin. Based on the known properties of these four insulins, the data provide suggestive evidence consistent with the hypothesis that there are subpopulations of antibodies recognizing regions on the insulin molecule that are well conserved, possibly the region involved in the formation of insulin dimers or receptor binding.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00254296
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  • 5
    Electronic Resource
    Electronic Resource
    Analysis of insulin receptors on human lymphoblastoid cell lines by flow cytometry (1984)
    Springer
    Diabetologia 27 (1984), S. 118-120 
    Details
    ISSN: 1432-0428
    Keywords: Insulin receptor ; flow cytometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Antibodies to the insulin receptor have provided important experimental probes of receptor structure and function. In the present study, we have characterized the insulin receptor on human lymphoblastoid cell lines using polyclonal and monoclonal anti-receptor antibodies and fluorescence flow cytometry. The cell lines were derived by Epstein-Barr virus transformation of peripheral mononuclear leucocytes from normal subjects or patients with disorders that affect the insulin receptor. Fluorescence analysis revealed a high level of specific fluorescence on lymphoid cell lines from normal individuals (mean peak fluorescence 30–50 units above the control) and was similar to the labelling of the spontaneously transformed lymphoblastoid cell line IM-9. Transformed cells from patients with syndromes of insulin resistance, such as the Rabson Mendenhall syndrome, leprechaunism and the type A syndrome of insulin resistance and acanthosis nigricans, exhibited little or no specific fluorescence. In all cases, there was a unimodal distribution of receptors on cells. In addition, there was a good correlation between specific binding of 125I-insulin and percentage peak fluorescence. The data indicate that fluorescence flow cytometry can be used to study the distribution of insulin receptor on different cell lines and to study cells derived from patients with disease states.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00275665
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  • 6
    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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