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  • 1
    Electronic Resource
    Electronic Resource
    On the pathogenesis of IDDM (1994)
    Springer
    Diabetologia 37 (1994), S. S82 
    Details
    ISSN: 1432-0428
    Keywords: Insulin-dependent diabetes mellitus ; free radicals ; cytokines ; beta-cell destruction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A model of the pathogenesis of insulin-dependent diabetes mellitus, i.e. the initial phase of beta-cell destruction, is proposed: in a cascade-like fashion efficient antigen presentation, unbalanced cytokine, secretion and poor beta-cell defence result in beta-cell destruction by toxic free radicals (O2 − and nitric oxide) produced by the beta cells themselves. This entire process is under polygenetic control.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400830
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Rapid changes in chromatographically determined haemoglobin A1c induced by short-term changes in glucose concentration (1980)
    Springer
    Diabetologia 19 (1980), S. 130-136 
    Details
    ISSN: 1432-0428
    Keywords: Haemoglobin A1c ; rapid glycosylation ; chromatography ; glucose ; 2-ketohexose derivatives ; artificial pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Chromatographically determined haemoglobin A1c concentration was measured during short-term (1–24 h) changes in glucose concentration in vitro and in vivo. In vitro at 37 °C the HbA1c concentration increased with glucose concentration and time both in normal and diabetic erythrocytes. In normal erythrocytes incubated in 20–100 mmol/l glucose, the increases in the HbA1c concentration were maximal after 4–6 h and then stable for the next 18–20 h. During the first hour, increases in the HbA1c concentration were linear with time and on average 0.034% HbA1c × h−1 × mmol/l glucose−1. In erythrocytes, after a rapidly produced increase (2h), HbA1c decreased to preincubation concentrations during a further incubation of the erythrocytes in a glucose-free medium at 37 °C for 4–6 h. The mean rate of linear decrease was 0.017% × h−1 × mmol/l glucose−1. After incubation of erythrocytes in 100 mmol/l glucose for 24 h, 1.3% HbA1c remained stable for 6 h in saline. The rapid increase in HbA1c concentration, as determined by chromatography, was not due to stable HbA1c (ketoamine linked glucose) as no increase was found in the HbA1c concentrations determined by the thiobarbiturate method. In juvenile diabetics controlled by an artificial beta-cell, rapid changes of blood glucose concentration (up to 20 mmol/l) resulted in increases in HbA1c concentration of as much as 1.9% within 12 h (mean 1.1%). Rapid in vivo increases in HbA1c concentration were reversible by normalization of the blood glucose concentration. That rapid changes in HbA1c may occur in daily diabetic life was evidenced by differences in HbA1c concentration between blood samples from out-patient diabetics incubated in saline for 16 hours at 4 °C and 37 °C (range of differences 0.2–1.4% HbA1c). The differences correlated to the blood glucose concentration at the time of sampling blood for HbA1c determination. Thus, incubation of blood at a low glucose concentration prior to determination of the glycosylated haemoglobin concentration may overcome interference from rapidly produced HbA1c.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00421859
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Heat shock protein induction in rat pancreatic islets by recombinant human interleukin 1β (1991)
    Springer
    Diabetologia 34 (1991), S. 150-156 
    Details
    ISSN: 1432-0428
    Keywords: Interleukin 1β ; islets of Langerhans ; heat shock proteins ; haem oxygenase ; free radicals ; Type 1 (insulin-dependent) diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Interleukin 1β, potentiated by tumour necrosis factor α, is cytotoxic to pancreatic Beta cells in vitro. We have hypothesized that interleukin 1β induces oxygen free radicals in Beta cells. Since cytotoxicity induced by free radicals and by heat may activate the same cellular repair mechanism (the heat shock response), the aim of this study was to investigate the pattern of protein synthesis in isolated islets after exposure to interleukin 1β (150 pg/ml, 24 h), tumour necrosis factor α (50 ng/ml, 24 h), heat shock (43°C, 30 min) and H2O2 (0.1 mmol/l, 20 min). By polyacrylamide gel electrophoresis, autoradiography, Western-blot analysis and partial peptide mapping of 35S-methionine labelled islets, interleukin 1β was found to induce a 73 kilodalton protein belonging to the heat shock protein family heat shock protein 70, a heat shock protein 90, and haem oxygenase. A minor induction of heat shock protein 73 and haem oxygenase was seen after H2O2. Interleukin 1β did not induce heat shock proteins in rat thyroid cells, rat mesangial cells or in human monocytes. Tumour necrosis factor α did not induce selective protein synthesis. Pre-exposure of islets to heat, tumour necrosis factor α, or H2O2 did not prevent the impairment of glucose-stimulated insulin release seen after 24 h of interleukin 1β exposure. The data are compatible with free radical induction by interleukin 1β. However, the heat shock response is not specific for oxidative injury, and previous studies have shown discrepant effects as to a protective effect of free radical scavengers against interleukin 1β-mediated beta-cytotoxicity. Thus, a role for free radicals in this context is not definitely proven.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418268
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    Paper (German National Licenses)
    Fulltext
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