Literature DB >> 12879252

Genetic control of non obese diabetic mice susceptibility to high-dose streptozotocin-induced diabetes.

C Gonzalez1, S Cuvellier, C Hue-Beauvais, M Lévi-Strauss.   

Abstract

AIMS/HYPOTHESIS: Streptozotocin is a monofunctional alkylating agent that induces diabetes in a large variety of mammals. While multiple low doses of streptozotocin induce immune-mediated diabetes, a single high dose of streptozotocin causes a strictly toxic diabetes. Among mouse strains, non-obese diabetic (NOD) mice are characterized by an extreme susceptibility to high dose of streptozotocin-induced diabetes whereas C3H/Or mice are particularly resistant. We hypothesized that NOD genes involved in high dose streptozotocin-induced diabetes could be also involved in the autoimmune destruction of pancreatic beta cells that characterizes this mouse strain which is a model of Type 1 diabetes.
METHODS: We carried out a whole genome linkage scan on a population of (C3H/Or x NOD) x NOD backcross 1 mice in order to identify the genetic loci involved in NOD susceptibility to high dose of streptozotocin-induced diabetes.
RESULTS: Two loci, in chromosome 9 (D9Mit135 marker, 48 cM) and in chromosome 11 (D11Mit286 marker, 52 cM), were associated with NOD susceptibility to high dose streptozotocin-induced diabetes, the latter being co-localized with the autoimmune diabetes-predisposing idd4 locus. Moreover, we report here that C57BL/6 mice deficient in Nitric Oxide Synthase 2 were as sensitive as wild-type C57BL/6 mice to high dose streptozotocin-induced diabetes. CONCLUSION/
INTERPRETATION: Although the Nitric Oxide Synthase 2 ( Nos2) gene, localized at 45.6 cM in chromosome 11, is a good candidate gene, our results suggest that Nitric Oxide Synthase 2 activation might not be a crucial event for streptozotocin-induced destruction of pancreatic beta cells.

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Year:  2003        PMID: 12879252     DOI: 10.1007/s00125-003-1168-7

Source DB:  PubMed          Journal:  Diabetologia        ISSN: 0012-186X            Impact factor:   10.122


  30 in total

Review 1.  Novel experimental strategies to prevent the development of type 1 diabetes mellitus.

Authors:  S Sandler; A K Andersson; A Barbu; C Hellerström; M Holstad; E Karlsson; J O Sandberg; E Strandell; J Saldeen; J Sternesjö; L Tillmar; D L Eizirik; M Flodström; N Welsh
Journal:  Ups J Med Sci       Date:  2000       Impact factor: 2.384

Review 2.  Genetic and immunological basis of autoimmune diabetes in the NOD mouse.

Authors:  K Yoshida; H Kikutani
Journal:  Rev Immunogenet       Date:  2000

3.  Congenic mapping of the diabetogenic locus Idd4 to a 5.2-cM region of chromosome 11 in NOD mice: identification of two potential candidate subloci.

Authors:  Marsha Grattan; Qing-Sheng Mi; Craig Meagher; Terry L Delovitch
Journal:  Diabetes       Date:  2002-01       Impact factor: 9.461

Review 4.  The action of NO and its role in autoimmune diabetes mellitus.

Authors:  K Fehsel; K D Kröncke; V Kolb-Bachofen
Journal:  Res Immunol       Date:  1995 Nov-Dec

5.  Androgen sensitization of streptozotocin-induced diabetes in mice.

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Journal:  Diabetes       Date:  1980-09       Impact factor: 9.461

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7.  Polygenic control of autoimmune diabetes in nonobese diabetic mice.

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8.  Streptozotocin-induced pancreatic insulitis: new model of diabetes mellitus.

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9.  Biochemical evidence for nitric oxide formation from streptozotocin in isolated pancreatic islets.

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10.  Inactivation of the poly(ADP-ribose) polymerase gene affects oxygen radical and nitric oxide toxicity in islet cells.

Authors:  B Heller; Z Q Wang; E F Wagner; J Radons; A Bürkle; K Fehsel; V Burkart; H Kolb
Journal:  J Biol Chem       Date:  1995-05-12       Impact factor: 5.157

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  5 in total

1.  Congenic mapping and candidate gene analysis for streptozotocin-induced diabetes susceptibility locus on mouse chromosome 11.

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3.  The Therapeutic Effect of Coriolus versicolor Fruiting Body on STZ-Induced ICR Diabetic Mice.

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4.  Verification That Mouse Chromosome 14 Is Responsible for Susceptibility to Streptozotocin in NSY Mice.

Authors:  Naru Babaya; Hironori Ueda; Shinsuke Noso; Yoshihisa Hiromine; Michiko Itoi-Babaya; Misato Kobayashi; Tomomi Fujisawa; Hiroshi Ikegami
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Review 5.  β-Cell failure in diabetes: Common susceptibility and mechanisms shared between type 1 and type 2 diabetes.

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