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  • 11
    Electronic Resource
    Electronic Resource
    An interleukin-1 receptor antagonist protein protects insulin-producing Beta cells against suppressive effects of interleukin-1β (1991)
    Springer
    Diabetologia 34 (1991), S. 445-448 
    Details
    ISSN: 1432-0428
    Keywords: Interleukin-1β ; interleukin 1 receptor ; insulin secretion ; pancreatic islets ; RINm5F cells ; insulin-dependent diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The cytokine interleukin-1β may have an important role in the autoimmune mediated damage of pancreatic Beta cells in insulin-dependent diabetes mellitus. In the present study we have investigated the effects of an interleukin-1 receptor antagonist protein, a blocker of the type I interleukin-1 receptor, on the suppressive actions of recombinant interleukin-1β on insulin-producing cells. Brief exposure (1–2 h) of rat and mouse pancreatic islets to 10 ng/ml recombinant interleukin-1β induced an 70–80% inhibition of insulin response to glucose after 12 h. These effects were completely counteracted by co-incubation with 100 ng/ml interleukin-1 receptor antagonist protein. When rat islets were cultured for 48 h in the presence of recombinant interleukin-1β (5 ng/ml) higher concentrations of interleukin-1 receptor antagonist protein (5000 ng/ml) were required to protect Beta-cell function. Interleukin-1 receptor antagonist protein also counteracted the inhibitory effects of recombinant interleukin-1β on the growth of the rat insulinoma cell line RINm5F. These data suggest that interleukin-1 receptor antagonist protein can protect insulin-producing cells from the deleterious effects of recombinant interleukin-1β, and that these cells possess type I interleukin-1 receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403185
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  • 12
    Electronic Resource
    Electronic Resource
    Human autoantibodies react with glutamic acid decarboxylase antigen in human and rat but not in mouse pancreatic islets (1993)
    Springer
    Diabetologia 36 (1993), S. 39-46 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 (insulin-dependent) diabetes mellitus ; autoantigen ; glutamic acid decarboxylase ; NOD mouse ; islets of Langerhans
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The presence of one of the major targets for auto-antibodies in Type 1 (insulin-dependent) diabetes mellitus, the enzyme glutamic acid decarboxylase, was studied in human, rat and mouse pancreatic tissue using immunoprecipitation and immunohistochemical techniques. Immunoprecipitation of glutamic acid decarboxylase was attempted with lysates of [35S]-methionine-labelled rat or mouse pancreatic islets using two different glutamic acid decarboxylase antisera, one mouse monoclonal antibody raised against the 65 kDa isoform of the enzyme, sera from six patients with Type 1 diabetes, one patient with stiff-man syndrome and sera from 19 non-obese diabetic mice. The same sera were used for immunoperoxidase staining of cryosections of human, rat or mouse pancreas. Using patient sera glutamic acid decarboxylase was detected by immunoprecipitations from isolated rat islets but not from islets of five different mouse strains tested, including the non-obese diabetic mouse. When using the non-obese diabetic mouse sera, glutamic acid decarboxylase could not be detected in either rat or mouse tissue. Immunoperoxidase staining demonstrated high levels of glutamic acid decarboxylase in human and rat pancreatic islets but low levels in mouse islets. Direct measurements of enzyme activity showed glutamic acid decarboxylase to be present in mouse islets at a level of about 40% of that in rat islets, and subsequent Western blot analyses indicated that mouse islets express the 67 kDa isoform, whereas in rat islets both the 67 and 65 kDa isoforms are present. The species difference at the level of one of the major islet cell autoantigens in Type 1 diabetes thus indicates that human or rat and mouse islets, respectively, express immunologically distinct forms of glutamic acid decarboxylase and differ in their way of regulating the enzyme production.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00399091
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  • 13
    Electronic Resource
    Electronic Resource
    Rapid deposition of amyloid in human islets transplanted into nude mice (1995)
    Springer
    Diabetologia 38 (1995), S. 543-549 
    Details
    ISSN: 1432-0428
    Keywords: Key words Islet amyloid polypeptide ; human pancreatic islets ; islet transplantation ; immune histochemistry ; hyperglycaemia.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Human islets of Langerhans were transplanted to the subcapsular space of the kidneys of nude mice which were either normoglycaemic or made diabetic with alloxan. After 2 weeks, the transplants were processed for light and electron microscopical analyses. In all transplants, islet amyloid polypeptide (IAPP)-positive cells were found with highest frequency in normoglycaemic animals. IAPP-positive amyloid was seen in 16 out of 22 transplants (73 %), either by polarisation microscopy after Congo red staining or by immune electron microscopy. At variance with previous findings of amyloid deposits exclusively in the extracellular space of islets of non-insulin-dependent diabetic patients, the grafted islets contained intracellular amyloid deposits as well. There was no clear difference in occurrence of amyloid between diabetic and non-diabetic animals. The present study indicates that human islets transplanted into nude mice very soon present IAPP-positive amyloid deposits. This technique may provide a valuable model for studies of the pathogenesis of islet amyloid and its impact on islet cell function. [Diabetologia (1995) 38: 543–549]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400722
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  • 14
    Electronic Resource
    Electronic Resource
    The harmony of the spheres: inducible nitric oxide synthase and related genes in pancreatic beta cells (1996)
    Springer
    Diabetologia 39 (1996), S. 875-890 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Nitric oxide ; nitric oxide synthase ; promoter ; transcription factor ; nuclear factor k B ; pancreatic islets ; beta cells ; insulin-producing cells ; insulin-dependent diabetes mellitus ; superoxide dismutase.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The radical nitric oxide (NO) is a possible mediator of pancreatic beta-cell damage in insulin-dependent diabetes mellitus (IDDM). NO is produced by the enzyme nitric oxide synthase (NOS), in a reaction where arginine is the main substrate. There are different isoforms of NOS, but in the context of immune mediated beta-cell damage the inducible form of NOS (iNOS) is the most relevant. The beta-cell iNOS is similar and encoded by the same gene on chromosome 17 as the iNOS expressed in macrophages and other nucleated cells. iNOS activation depends on gene transcription and de novo enzyme synthesis, and NO seems to induce a negative feedback on iNOS expression. While iNOS mRNA is induced by interleukin-1β (IL-1β ) alone in rodent insulin-producing cells, a combination of two (IL-1β + interferon γ) (IFN-γ ) or three (IL-1β + IFNγ + tumour necrosis factor α) cytokines is required for iNOS activation in human pancreatic islets. The promoter region of the murine iNOS gene has at least 25 binding sites for different transcription factors, and the nuclear transcription factor k B is necessary for cytokine-induced iNOS transcription in both rodent and human pancreatic islets. The nature of other transcription factors relevant for iNOS regulation in these cells remains to be determined. Induction of iNOS is paralleled by induction of several other cytokine-dependent genes in beta cells, including argininosuccinate synthetase, cyclooxygenase and manganese superoxide dismutase. Some of these genes may contribute to beta-cell damage, while others are probably involved in beta-cell defence and/or repair. Regulation of iNOS and other related genes in beta cells is complex, and differs in several aspects from that observed in macrophages. There are also important differences in iNOS regulation between rodent and human pancreatic islets. A detailed knowledge of the molecular regulation of these genes in beta cells may be instrumental in the development of new approaches to prevent beta-cell destruction in early IDDM. [Diabetologia (1996) 39: 875–890]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403906
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  • 15
    Electronic Resource
    Electronic Resource
    Regulation by cytokines of the inducible nitric oxide synthase promoter in insulin-producing cells (1998)
    Springer
    Diabetologia 41 (1998), S. 1101-1108 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Nitric oxide ; iNOS ; NF-kB ; beta-cells ; interleukin-1 ; diabetes mellitus.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cytokines could contribute to beta-cell damage in Type I diabetes mellitus. The radical nitric oxide, generated by the inducible form of nitric oxide synthase (iNOS), is a potential mediator of cytokine-induced beta-cell dysfunction. In rat pancreatic islets and insulin-producing cell lines, interleukin-1β (IL-1β) induces expression of iNOS mRNA and increases NO production, an effect potentiated by interferon-γ (IFN-γ). In human islet cells both IL-1β and IFN-γ are required for iNOS expression. We have shown previously that both the transcription factors nuclear factor-kB (NF-kB) and interferon regulatory factor-1 (IRF-1) are activated by cytokines in rodent and human islets but there is no direct information on the regulation of the iNOS promoter in insulin-producing cells. We presently investigated the effects of cytokines on iNOS transcriptional regulation in both rat insulin-producing RINm5F cells and in primary FACS-purified rat beta cells. Transient transfection experiments with the 1.5-kb rat promoter region and 5 ′ deletants of it showed that a distal region extending up to –1002 bp, and containing a distal and a proximal nuclear factor-kB (NF-kB) binding site, a γ-interferon activated site (GAS) and two adjacent IFN-stimulated response elements (ISRE), is required for IL-1β induction and IFN-γ potentiation of iNOS activation. Site-mutation analysis showed that both the distal and proximal NF-kB and GAS are necessary for IL-1β-induced iNOS expression in RINm5F cells. In these cells IFN-γ potentiation is mostly mediated by GAS and ISRE, suggesting a role for the IFN-γ-induced transcription factors Stat1α (which binds GAS) and IRF-1 (which binds ISRE), which may cooperate with NF-kB induced by IL-1β for iNOS activation. In primary beta cells both NF-kB binding sites are required for IL-1β-induced iNOS promoter activation. In these cells IFN-γ neither increased IL-1β-induced iNOS promoter activity nor iNOS mRNA expression but it induced a twofold increase in NO production. The present results unveiled the nature of the promoter binding sites necessary for iNOS expression in rodent beta cells. This information could be relevant for the development of new strategies aimed at preventing cytokine-induced iNOS expression and consequent beta-cell damage. [Diabetologia (1998) 41: 1101–1108]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051036
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