reflect immune system dysregulation ( Van Belle et al . 2009 ). Therefore, studies utilizing alternative models to address the roles of Nrf2 signaling in autoimmune-based diabetes are needed. Non-obese diabetic (NOD) mice have been used widely as a
Yoko Yagishita, Akira Uruno, Dionysios V Chartoumpekis, Thomas W Kensler and Masayuki Yamamoto
Ke Ke, Ok-Joo Sul, Soo-Wol Chung, Jae-Hee Suh and Hye-Seon Choi
loss by amplifying RANKL-induced signaling in OCs. Materials and methods Animals and study design Nod2 − / − ( Nod2 -knockout (KO)) mice were purchased from the Jackson Laboratory. The mice were bred with C57BL/6J mice and maintained by
Elizabeth S Barrie, Mels Lodder, Paul H Weinreb, Jill Buss, Amer Rajab, Christopher Adin, Qing-Sheng Mi and Gregg A Hadley
Introduction Type 1 diabetes is a T cell-mediated autoimmune disease caused by the destruction of insulin-producing β cells of the islets of Langerhans in the pancreas, resulting in a hyperglycemic state. Non-obese diabetic (NOD) mice (NOD
Astrid Chamson-Reig, Edith J Arany, Kelly Summers and David J Hill
NOD mouse and BioBreeding (BB) rat ( Lefebvre et al . 2006 ). However, food antigens can also interact with the gut immune system, resulting in a Th1 cytokine pattern of expression within the Peyer's patches of young NOD mice ( Chakir et al . 2005
Jacob Jelsing, Niels Vrang, Søren B van Witteloostuijn, Michael Mark and Thomas Klein
as add-on therapy to insulin in reducing BG levels in a small sample of patients with T1D. In addition, sitagliptin was shown to preserve islet transplants in non-obese diabetic (NOD) mice ( Kim et al . 2009 , 2010 ). This mouse model spontaneously
Jane A Mitchell, Mark J Paul-Clark, Graham W Clarke, Shaun K McMaster and Neil Cartwright
including NFκB and AP-1. PRRs include transmembrane toll-like receptors (TLRs) and cytosolic nucleotide oligomerisation domain (NOD) proteins containing leucine-rich repeats (NLRs). Bacterial LPS and its effects on biological systems
Jon G Mabley, Pal Pacher, Kanneganti G K Murthy, William Williams, Garry J Southan, Andrew L Salzman and Csaba Szabo
following sources. Amplex red xanthine/xanthine oxidase assay kits were obtained from Molecular Probes (Eugene, OR, USA). Streptozotocin and sodium citrate were obtained from Sigma. BALB/c and NOD mice were purchased from Taconic (Germantown, NY, USA
Guofeng Zhang, Hiroki Hirai, Tao Cai, Junnosuke Miura, Ping Yu, Hanxia Huang, Martin R Schiller, William D Swaim, Richard D Leapman and Abner L Notkins
was increased at 60 min, was highest at 90 min (Fig. 4D ), and decreased thereafter (not shown). RESP18 protein also was increased in the islets of NOD mice following the development of diabetes. Western blots showed a tenfold increase at 2 days after
A Amrani, M Jafarian-Tehrani, P Mormède, S Durant, J-M Pleau, F Haour, M Dardenne and F Homo-Delarche
Cytokines, particularly interleukin 1 (IL-1) and tumor necrosis factor, are known to induce hypoglycemia in normal rodents or different experimental models of type II diabetes. We investigated, at the pre-diabetic stage, the effect of short-term administration of murine recombinant interleukin-1α (mrIL-1α) on the levels of glucose, insulin and corticosterone in the non-obese diabetic (NOD) mouse, a spontaneous model of type I diabetes. Two-month-old, pre-diabetic NOD mice of both sexes were insensitive to mrIL-1α (12·5 and 50 μg/kg) 2 h after administration, the time at which the maximal decrease (around 50%) was observed in the C57BL/6 mouse strain. Kinetic studies however showed that mrIL-1α lowered glycemia in both sexes of NOD mice, but the effect was limited and delayed. In the NOD and C57BL/6 strains, mrIL-1α had no influence on insulin levels in females, but significantly increased them in males (P<0·0001). Castration of NOD males abrogated the stimulatory effect of mrIL-1α on insulin secretion. Corticosterone secretion was stimulated by mrIL-1α in both sexes of NOD and C57BL/6 mice, and this effect was faster and greater in NOD females than in C57BL/6 females. The incomplete hypoglycemic response to mrIL-1α in females may be attributed to the anti-insulin effect of glucocorticoids, an effect which can be demonstrated when mrIL-1α is administered to adrenalectomized animals or when mrIL-1α is administered together with the glucocorticoid antagonist RU38486. In NOD males, in contrast, glucocorticoids did not play a major role in the limited hypoglycemic response to mrIL-1α, since RU38486 and adrenalectomy were not able to unmask a hypoglycemic effect. Moreover, NOD mice of both sexes were less sensitive than C57BL/6 mice to the hypoglycemic effect of insulin (2·5 U/kg), which suggests some degree of insulin-resistance in NOD mice. With regard to the effect of IL-1 on NOD mouse glycemia, therefore, these results suggest that glucocorticoids and/or androgens, according to the animal's sex, may induce a state of insulin-resistance.
Journal of Endocrinology (1996) 148, 139–148
M-C Many, S Maniratunga, I Varis, M Dardenne, H A Drexhage and J-F Denef
The administration of a high iodide dose (HID; 10 μg/day) to goitrous mice is known to induce thyroid cell necrosis and inflammation, which, in most strains, is transient. In this study, we analyzed the effects of iodide in autoimmune prone non-obese diabetic (NOD) mice.
Control NOD mice fed a standard diet (MID; 1 μg I/day) or HID did not spontaneously develop thyroiditis. In NOD mice previously made goitrous, HID provoked thyroid cell necrosis and diffuse inflammation within 4 days. Inflammatory cells consisted of MHC-class II+ antigen-presenting cells, CD4+ T helper cells and CD8+ T suppressor/cytotoxic cells. After 96 days of treatment with HID, thyroiditis similar to Hashimoto's disease was obtained in 100% of the animals, with destruction of thyroid follicles, large clusters of T and B cells, and antithyroid antibodies in the plasma. When treating goitrous mice with MID, no cell necrosis was observed and no autoimmune thyroiditis was obtained. The early iodide-induced cell necrosis and inflammation may thus be considered as an important factor in the induction and persistence of autoimmune thyroiditis in individuals carrying a genetic susceptibility to autoimmune disease.
Journal of Endocrinology (1995) 147, 311–320