Susceptibility to streptozotocin-induced diabetes is mapped to mouse chromosome 11

Babaya, Naru; Ikegami, Hiroshi; Fujisawa, Tomomi; Nojima, K.; Itoi-Babaya, Michiko; Inoué, Kaori; Ohno, Tamio; Shibata, Masao; Ogihara, Toshio

doi:10.1016/j.bbrc.2004.12.149

Cited by 22 publications

(31 citation statements)

References 37 publications

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“…We previously reported sequence analyses of the genes for hepatocyte nuclear factor-1β, GLUT4 and nucleoredoxin [6,7,[38][39][40]. In this study, we determined the nucleotide sequences of Gck, which is mapped in the centromeric region of Chr11.…”

Section: Discussionmentioning

confidence: 99%

Direct evidence for susceptibility genes for type 2 diabetes on mouse chromosomes 11 and 14

et al. 2010

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These data provide direct evidence that Chr11 and Chr14 harbour major susceptibility genes for type 2 diabetes. These two chromosomes interact to cause more severe hyperglycaemia and obesity, which was not observed with the presence of either single chromosome, indicating different modes of gene-gene interaction depending on the phenotype. Marked changes in the phenotypes retained in the consomic strains will facilitate fine mapping and the identification of the responsible genes and their interaction with each other, other genes and environmental factors.

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Section: Discussionmentioning

confidence: 99%

Direct evidence for susceptibility genes for type 2 diabetes on mouse chromosomes 11 and 14

et al. 2010

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“…In addition, the following evidence suggests that adoption of STZ-induced diabetes model in this study is appropriate: Firstly, multiple low dose of STZ-induced diabetes is a well-characterized T cell-mediated autoimmune diabetes (16–17, 26); secondly, the susceptibility genes of mice to STZ-induced diabetes are mapped to the same gene loci that are responsible for development of spontaneous diabetes in NOD mice (27), suggesting the similarity of autoimmune mechanism in contributing to the development of diabetes in both models; thirdly, the potential role of Tregs in suppression of STZ-induced diabetes has been reported (11). …”

Section: Discussionmentioning

confidence: 99%

CD25^high T Cells with a Prolonged Survival Inhibit Development of Diabetes

Yan¹,

Xiong²,

Zhang³

et al. 2008

Int J Immunopathol Pharmacol

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The goal of this study is to examine a novel hypothesis that the progression of diabetes is partially due to the weakened survival of CD25high T cells, and prolonging survival of CD25high T cells inhibits the development of diabetes. Since CD28 co-stimulation is essential for the survival of CD4+CD25high T cells, we determined whether CD28-upregulated translationally controlled tumor protein (TCTP) prolongs the survival of CD4+CD25high regulatory T cells (Tregs) by a transgenic approach. The TCTP transgene prevents Tregs from undergoing apoptosis induced by Interleukin-2 withdrawal-, dexamethasone-, cyclophosphamide-, and anti-Fas treatment in vitro. In addition, transgenic Tregs express higher levels of FOXP3 than wild-type counterparts and maintain suppressive activity, suggesting that TCTP promotes Tregs escape from thymic negative selection, and that prolonged survival does not attenuate Treg suppression. Moreover, TCTP transgenic Tregs inhibit the development of autoimmune diabetes due to increased survival of suppressive Tregs and decreased expression of pancreatic TNF-α. Promoting the survival of CD25high T cells leads to prolonged survival of Tregs but not activated CD25+ non-Treg T cells. Thus, we propose a new model of “two phase survival” for Tregs. Our results suggest that modulation of Treg survival can be developed as a new therapy for autoimmune diseases.

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“…We are surprised that there is not compensation for insulin deficiency with the single copy of Ins1 and with two copies of Ins1. However, a strain derived from the same colony as the NOD mouse, the NagoyaShibata-Yasuda mouse [9,10], a model of type 2 diabetes, which may share background genome with NOD [11,12], has no compensational hypertrophy of pancreatic islets despite increasing insulin resistance with ageing [9]. In addition, Kulkarni et al reported the importance of background genome in the induction of type 2 diabetes [13].…”

Section: Discussionmentioning

confidence: 99%

A new model of insulin-deficient diabetes: male NOD mice with a single copy of Ins1 and no Ins2

Babaya¹,

Nakayama²,

Moriyama

et al. 2006

Diabetologia

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Susceptibility to streptozotocin-induced diabetes is mapped to mouse chromosome 11

Cited by 22 publications

References 37 publications

Direct evidence for susceptibility genes for type 2 diabetes on mouse chromosomes 11 and 14

Direct evidence for susceptibility genes for type 2 diabetes on mouse chromosomes 11 and 14

CD25^high T Cells with a Prolonged Survival Inhibit Development of Diabetes

A new model of insulin-deficient diabetes: male NOD mice with a single copy of Ins1 and no Ins2

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Susceptibility to streptozotocin-induced diabetes is mapped to mouse chromosome 11

Cited by 22 publications

References 37 publications

Direct evidence for susceptibility genes for type 2 diabetes on mouse chromosomes 11 and 14

Direct evidence for susceptibility genes for type 2 diabetes on mouse chromosomes 11 and 14

CD25high T Cells with a Prolonged Survival Inhibit Development of Diabetes

A new model of insulin-deficient diabetes: male NOD mice with a single copy of Ins1 and no Ins2

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Product

Resources

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CD25^high T Cells with a Prolonged Survival Inhibit Development of Diabetes