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Title of Journal: Diabetologia

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Abbravation: Diabetologia

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Springer-Verlag

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DOI

10.1016/j.ajog.2016.02.030

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1432-0428

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The BioBreeding rat diabetes model is infected wit

Authors: Bo Niklasson T Hultman R Kallies M Niedrig R Nilsson PO Berggren L JunttiBerggren S Efendic A Lernmark W Klitz
Publish Date: 2007/04/04
Volume: 50, Issue: 7, Pages: 1559-
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Abstract

To the Editor A useful tool for understanding the pathogenesis of human diseases has been the use of animal models The BioBreeding BB rat has been a useful source of knowledge for type 1 diabetes with over 1400 publications recorded in PubMed We now present evidence that this animal model is infected with a picornavirusWe previously reported the covariation of the incidence of type 1 diabetes and the 3–4 year population cycles of the bank vole Clethrionomys glareolus in Sweden 1 This led us to hypothesise that the bank vole is the reservoir and/or vector of an infectious agent causing this disease in a predisposed population of humans The hypothesis was supported by the observation that wildtrapped bank voles developed symptoms of diabetes in captivity 2 A novel picornavirus Ljungan virus LV has been isolated from diabetic bank voles in Sweden Furthermore viral antigen and picorna virallike particles were detected by immunohistochemistry IHC and electron microscopy in affected pancreatic beta cells 2 3 Analysis of new and stored samples have shown that LV is also present in wild voles in Denmark and the USA 4 In addition we have recently reported that clinical diabetes occurs in several other species of wild voles and lemmings in northern Sweden extending the host range of LV suggesting that this virus may cause significant morbidity among wild small rodents in general 5 Outbred CD1 laboratory mice develop glucose intolerance at 10–15 weeks of age following exposure to LV in utero or shortly after birth 6 The wide host range of LV the association with diabetes in wild rodents and the finding that LV induces glucose intolerance under controlled conditions in laboratory mice led us to investigate the BB ratAll experimental procedures described below were approved by the animal ethics committee in Stockholm N9/05 and in accordance with international guidelines NIH publications no 8523 revised 1985 Formalinfixed paraffinembedded pancreas tissue was stained using IHC We used LV VP1specific polyclonal rabbit antisera and a mouse monoclonal antibody reactive to all known LV isolates but not to parecho or cardiovirus We also used three independent realtime RTPCR assays to identify and quantify LV infection One PCR assay used primers and two different minorgroovebinder probes designed to amplify a 187 bp PCR product from the 5′ untranslated region of the LV genome In addition we used primers designed to amplify a 103 bp PCR product from the 5′ untranslated region and a 164 bp product from the 2A region of the LV genome followed by a melting point analysis at the end of the amplificationBeta cell islet and adjacent acini from a nondiabetic BB rat pancreas at 40 days of age The islet is stained with an LVspecific monoclonal antibody red and the background is stained with methyl green Negative control normal mouse serum showed no LVspecific staining The specific staining could be blocked with LV antigen but not with control antigenAdditionally ten Wistar and five Sprague–Dawley rats from Sweden Scanbur Sollentuna also tested positive for LV by IHC staining indicating that the virus may be found in several possibly all strains of rats The presence of LV in samples from rats from Sweden and the US suggests that LV may be characteristic of the strains and populations tested rather than reflecting incidental infections at single locations We present no data generated from BB rats directly proving that LV is involved in the development of the disease in these animals but the evidence from native rodents and the causative role for LV in diabetes in a CD1 mouse model show that LV may itself be a pathogenic agent of diabetes Studies are under way to determine whether specific antiviral therapy can alter the clinical outcome of BB ratsThe demonstration that BB rats are infected with LV suggests that this animal model of spontaneous diabetes needs to be reconsidered Additional work is needed to extend the findings of this study to the larger context of rodent susceptibility and carriage of LV including the human commensal Rattus norvegicus and its laboratory strains Regardless of the wider implications of this finding it is clearly essential that a common pathogen with the potential to cause or interfere with disease development must be placed under exacting experimental control in an animal disease model


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  1. Oral probiotic administration induces interleukin-10 production and prevents spontaneous autoimmune diabetes in the non-obese diabetic mouse
  2. Glycated albumin but not HbA 1c reflects glycaemic control in patients with neonatal diabetes mellitus
  3. Comparison of high-fat and high-protein diets with a high-carbohydrate diet in insulin-resistant obese women
  4. Lack of association between gene variants in the ALMS1 gene and Type 2 diabetes mellitus
  5. Lack of association between gene variants in the ALMS1 gene and Type 2 diabetes mellitus
  6. Low-density-lipoprotein cholesterol concentrations and risk of incident diabetes: epidemiological and genetic insights from the Framingham Heart Study
  7. AMPK phosphorylation of ACC2 is required for skeletal muscle fatty acid oxidation and insulin sensitivity in mice
  8. Effects of fenofibrate on renal function in patients with type 2 diabetes mellitus: the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) Study
  9. Angiotensin-I converting enzyme insertion/deletion polymorphism and its association with diabetic nephropathy: a meta-analysis of studies reported between 1994 and 2004 and comprising 14,727 subjects
  10. Microarray analysis of genes with impaired insulin regulation in the skeletal muscle of type 2 diabetic patients indicates the involvement of basic helix-loop-helix domain-containing, class B, 2 protein (BHLHB2)
  11. Amino acids require glucose to enhance, through phosphoinositide-dependent protein kinase 1, the insulin-activated protein kinase B cascade in insulin-resistant rat adipocytes
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  13. Prevalence and 25 year incidence of proliferative retinopathy among Danish type 1 diabetic patients
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  20. Metabolic and hormonal response to intermittent high-intensity and continuous moderate intensity exercise in individuals with type 1 diabetes: a randomised crossover study
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  22. Induction of the chemokine interferon-γ-inducible protein-10 in human pancreatic islets during enterovirus infection
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  24. Glucose tolerance and insulin resistance in Indian children: relationship to infant feeding pattern
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  26. An RBP4 promoter polymorphism increases risk of type 2 diabetes
  27. Müller glial dysfunction during diabetic retinopathy in rats is linked to accumulation of advanced glycation end-products and advanced lipoxidation end-products
  28. WNT/β-catenin increases the production of incretins by entero-endocrine cells
  29. Enhanced susceptibility of Cpt1c knockout mice to glucose intolerance induced by a high-fat diet involves elevated hepatic gluconeogenesis and decreased skeletal muscle glucose uptake
  30. Is rs34861192 or rs1862513 a more promising variant for determining plasma resistin in an aged Japanese population?
  31. Environmental pollutants and type 2 diabetes: a review of mechanisms that can disrupt beta cell function
  32. Reply to comment on: Høi-Hansen T, Pedersen-Bjergaard U, Thorsteinsson B (2005) The Somogyi phenomenon revisited using continuous glucose monitoring in daily life. Diabetologia 48:2437–2438
  33. The prevalence of insulin autoantibodies at the onset of Type 1 diabetes is higher in males than females during adolescence
  34. Anaemia in diabetes: is there a rationale to TREAT?
  35. —to: Hales CN, Ozanne SE (2003) For Debate: Fetal and early postnatal growth restriction lead to diabetes, the metabolic syndrome and renal failure. Diabetologia 46:1013–1019
  36. Causal interpretation requires appropriate study design. Reply to Priest PC [letter]
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  44. Adenovirus-mediated overexpression of Tcfe3 ameliorates hyperglycaemia in a mouse model of diabetes by upregulating glucokinase in the liver
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  47. A longitudinal study of iron status during pregnancy and the risk of gestational diabetes: findings from a prospective, multiracial cohort
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  50. Harry Keen, 1925–2013
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  53. R. Tattersall. Diabetes: the biography. Oxford University Press, Oxford, 2009
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  58. Early life treatment with vancomycin propagates Akkermansia muciniphila and reduces diabetes incidence in the NOD mouse
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  61. Low TCR signal strength induces combined expansion of Th2 and regulatory T cell populations that protect mice from the development of type 1 diabetes
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  85. Comment on: Nathan DM, Buse JB, Davidson MB et al (2006) Management of hyperglycaemia in type 2 diabetes: a consensus algorithm for the initiation and adjustment of therapy. A consensus statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetologia 49:1711–1721
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