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  • 1
    Digitale Medien
    Digitale Medien
    Springer
    Diabetologia 36 (1993), S. 912-919 
    ISSN: 1432-0428
    Schlagwort(e): BBZ/Wor ; obesity ; autoimmune diabetes mellitus
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The BBZ/Wor rat is a model of obesity and autoimmune diabetes mellitus developed by crossing the BB/Wor and Zucker rats. We studied circulating glucose and insulin levels, islet morphology and lymphocyte subsets in lean and obese BBZ/Wor rats before and after the onset of diabetes, and studied the clinical course of diabetes in animals after interruption of exogenous insulin therapy. Lean BBZ/Wor rats developed insulin-dependent diabetes and died in ketoacidosis within 1 week after cessation of insulin injections. Diabetes also developed in obese rats, but these animals were not insulin-dependent and survived for months without insulin therapy. The islets of the lean diabetic rats revealed complete destruction of pancreatic beta cells and plasma insulin levels were virtually undetectable. In contrast, the islets of the obese rats revealed insulitis and substantial beta-cell loss, however autoimmune bete-cell destruction was incomplete, and residual beta cells were presumably responsible for the presence of measurable levels of plasma insulin and the long-term survival of obese diabetics without insulin therapy. Obese rats were hyperinsulinaemic, developed diabetes significantly earlier, and with a greater incidence than lean rats, suggesting a possible relationship between enhanced beta-cell metabolic activity and immune destruction. Obese males became diabetic more frequently and at an earlier age than obese females and lean rats of both sexes, suggesting a role for gender in the pathogenesis of diabetes. We conclude that the BBZ/Wor rat is a unique animal model for investigating the interaction of obesity, beta-cell metabolism, autoimmune insulitis and genetic predisposition to diabetes.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1432-0428
    Schlagwort(e): GLUT 2 ; BB/Wor rats ; Kilham Rat Virus ; autoimmune diabetes mellitus ; beta cell ; islets of Langerhans ; parvoviridae infections
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Loss of GLUT 2, the glucose transporter isoform of pancreatic beta cells, has been reported to accompany the onset and perhaps contribute to the pathogenesis, of insulin-dependent and non-insulin-dependent diabetes mellitus in BB/Wor and Zucker fatty rats. In this study we investigated the effect of Kilham Rat Virus infection on GLUT 2 expression in diabetes-resistant BB/Wor rats. Viral antibodyfree diabetes-resistant rats do not develop spontaneous diabetes, but inoculation with Kilham Rat Virus induces autoimmune beta-cell destruction and hyperglycaemia. Pancreas sections from normoglycaemic diabetes-resistant BB/Wor rats were obtained 5, 7 and 25 days after inoculation with Kilham Rat Virus and stained for GLUT 2 using a rabbit polyclonal antibody. At all time points, beta cells displayed GLUT 2 expression comparable to uninfected diabetes-resistant controls. Immunostained insulin content of the beta cells also remained unchanged. Sections were also examined from Kilham Rat Virus inoculated diabetes-resistant rats with lymphocytic insulitis or diabetes. GLUT 2 and insulin immunostaining were unchanged in non-diabetic rats with early insulitis. GLUT 2 beta-cell staining was variably reduced in diabetic rats with established insulitis and reduced beta-cell insulin immunostaining. Hence, the initial stages of Kilham Rat Virus-induced diabetes in diabetes-resistant rats are not accompanied by a significant reduction in GLUT 2 expression. These results suggest that the loss of GLUT 2 does not play a significant role in the aetiology of diabetes in the Kilham Rat Virus-infected diabetes-resistant BB/Wor rat.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    ISSN: 1432-0428
    Schlagwort(e): Key words GLUT 2 ; BB/Wor rats ; Kilham Rat Virus ; autoimmune diabetes mellitus ; beta cell ; islets of Langerhans ; parvoviridae infections.
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Loss of GLUT 2, the glucose transporter isoform of pancreatic beta cells, has been reported to accompany the onset and perhaps contribute to the pathogenesis, of insulin-dependent and non-insulin-dependent diabetes mellitus in BB/Wor and Zucker fatty rats. In this study we investigated the effect of Kilham Rat Virus infection on GLUT 2 expression in diabetes-resistant BB/Wor rats. Viral antibody-free diabetes-resistant rats do not develop spontaneous diabetes, but inoculation with Kilham Rat Virus induces autoimmune beta-cell destruction and hyperglycaemia. Pancreas sections from normoglycaemic diabetes-resistant BB/Wor rats were obtained 5, 7 and 25 days after inoculation with Kilham Rat Virus and stained for GLUT 2 using a rabbit polyclonal antibody. At all time points, beta cells displayed GLUT 2 expression comparable to uninfected diabetes-resistant controls. Immunostained insulin content of the beta cells also remained unchanged. Sections were also examined from Kilham Rat Virus inoculated diabetes-resistant rats with lymphocytic insulitis or diabetes. GLUT 2 and insulin immunostaining were unchanged in non-diabetic rats with early insulitis. GLUT 2 beta-cell staining was variably reduced in diabetic rats with established insulitis and reduced beta-cell insulin immunostaining. Hence, the initial stages of Kilham Rat Virus-induced diabetes in diabetes-resistant rats are not accompanied by a significant reduction in GLUT 2 expression. These results suggest that the loss of GLUT 2 does not play a significant role in the aetiology of diabetes in the Kilham Rat Virus-infected diabetes-resistant BB/Wor rat. [Diabetologia (1994) 37: 1186–1194]
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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