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  • 1
    Electronic Resource
    Electronic Resource
    The HIV-1 protease inhibitor indinavir impairs insulin signalling in HepG2 hepatoma cells (2000)
    Springer
    Diabetologia 43 (2000), S. 1145-1148 
    Details
    ISSN: 1432-0428
    Keywords: Keywords HIV protease inhibitors ; lipodystrophy syndrome ; diabetes mellitus ; insulin resistance ; insulin signalling.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Patients treated with human immunodeficiency virus-1 protease inhibitors often develop impaired glucose tolerance or diabetes, most likely due to an induction of insulin resistance. We therefore investigated whether the protease inhibitor indinavir alters insulin signalling. Methods. We incubated HepG2 cells for 48 h without or with indinavir (100 μmol/l). Subsequently 125I-insulin binding to the cells and the effects of insulin stimulation on insulin-receptor substrate-1-phosphorylation, association of phosphatidylinositol 3-kinase with insulin-receptor substrate-1 and Akt-Thr308-phosphorylation were measured. Results. In cells not exposed to indinavir, insulin (100 nmol/l) led to rapid increases of insulin-receptor substrate-1-phosphorylation, association of phosphatidylinositol 3-kinase with insulin-receptor substrate-1 and Akt-phosphorylation during the first 75 s, followed by subsequent decreases. In indinavir-treated cells, these insulin-stimulated increases during the first 75 s were reduced by 30–60 % and this was not associated with alterations in cell number or viability, insulin binding to the cells or cellular insulin-receptor substrate-1-content. Conclusion/interpretation. Effects of indinavir on initial insulin signalling could cause, or contribute to, the metabolic effects of human immunodeficiency virus-1 protease inhibitors. [Diabetologia (2000) 43: 1145–1148]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051505
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  • 2
    Electronic Resource
    Electronic Resource
    Fas (CD95) expression on CD4+ T cells from HIV-infected patients increases with disease progression (1995)
    Springer
    Journal of molecular medicine 73 (1995), S. 591-593 
    Details
    ISSN: 1432-1440
    Keywords: Acquired immunodeficiency syndrome ; Human immundeficiency virus ; Apoptosis ; Fas antigen (CD95) ; p24 antigen ; Immune complex dissociation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Active T cell suicide (apoptosis) is supposed to be involved in the CD4+ T cell depletion in the course of HIV infection. We investigated the expression of the apoptosis-related antigen Fas on CD4+ T cells from 25 HIV-positive individuals (CDC I-III) and 8 HIV-negative controls by two-colour flowcytometry. In addition, we evaluated: total CD4 count, HIV p24 antigen concentration in serum after immune complex dissociation, and clinical course of infection in HIV-positive individuals. We found a significant increase in mean Fas expression on CD4+ T cells from HIV-positive individuals compared to HIV-negative individuals (85.84±14.92% vs. 64.28±7.59%, P〈0.001). Within the HIV-positive group the increase in Fas expression was correlated with the decline in CD4 count (r=−0.76, P〈0.001), p24 antigen concentration in serum after immune complex dissociation (r=0.67, P〈0.001), and CDC stage (r=0.73, P〈0.001). The upregulation of Fas antigen on CD4 cells is associated with CD4 depletion and other virological and clinical marker of disease progression in HIV infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00196352
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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