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Yoko Yagishita, Akira Uruno, Dionysios V Chartoumpekis, Thomas W Kensler, and Masayuki Yamamoto

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

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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

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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

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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

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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

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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

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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

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Wenjuan Liu, Harry Kevin Lau, Dong Ok Son, Tianru Jin, Yehong Yang, Zhaoyun Zhang, Yiming Li, Gerald J Prud’homme, and Qinghua Wang

/or decreasing apoptosis. However, comparable studies have not been performed with human islets. To test our hypothesis for the existence of a collaborative effect, we transplanted a suboptimal number of human islets into diabetic immunodeficient NOD

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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

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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