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Xuemei Tang, Jingwen Li, Wei Xiang, Ye Cui, Bin Xie, Xiaodong Wang, Zihui Xu, and Lixia Gan

, as is the case for fasting ( Chan et al . 2002 ), food deprivation ( Cohen et al . 2005 ), type 1 diabetes ( Kratzsch et al . 2004 , Kratzsch et al . 2006 ), eating disorders such as anorexia nervosa and bulimia nervosa ( Monteleone et al . 2002

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K Goosse, T Bouckenooghe, M Balteau, B Reusens, and C Remacle

β-cell toxicity in type-1 diabetes ( Loweth et al . 1998 , Amrani et al . 2000 , Augstein et al . 2003 ), we also measured the expression of the mRNA coding for the receptor in the islets of the four groups ( Fig. 2 ). Cytokines increased Fas

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Antonella Amato, Sara Baldassano, and Flavia Mulè

is able to delay the onset of insulin resistance ( Baldassano et al. 2016 a ). Indeed, a previous study has described the failure of GLP2 to modify diabetes onset in non-obese diabetic mouse, a model of type 1 diabetes (T1D) ( Hadjiyanni et al

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Risheng Ye, Min Ni, Miao Wang, Shengzhan Luo, Genyuan Zhu, Robert H Chow, and Amy S Lee

. 2005 ). Furthermore, variations within IP3R3 have been identified as a risk factor for type 1 diabetes in humans ( Roach et al . 2006 ). IP3R1 is the most abundant isoform in mouse brain and pancreatic β-cells ( De Smedt et al . 1997 , Lee & Laychock

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Jeffrey Friedman

efficacy for the treatment of type 1 diabetes. This possibility has now been tested in streptozotocin-treated mice who are either partial or completely insulin deficient. In both cases, leptin markedly lowered blood glucose. Indeed in one study, untreated

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Xuefeng Yang, Shuang Mei, Haihua Gu, Huailan Guo, Longying Zha, Junwei Cai, Xuefeng Li, Zhenqi Liu, and Wenhong Cao

proteins/amino acids. Thus, we have recently addressed several simple questions. First, does glucose itself cause insulin resistance in the absence of insulin? Our results show that animals with untreated hyperglycemia in type 1 diabetes mellitus (T1DM

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Jessica L Huang, Sharon Lee, Pelle Hoek, Talitha van der Meulen, Richard Van, and Mark O Huising

reported to be decreased in senescent beta cells in type 1 diabetes ( Thompson et al. 2019 ). The fact that UCN3 expression tracks closely with beta cell function across different beta cell states raises the question if UCN3 is merely a marker of mature

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Luiz F Rezende, Luiz F Stoppiglia, Kleber L A Souza, Alessandro Negro, Francesco Langone, and Antonio C Boschero

through activation of voltage-dependent Ca 2+ channels. The rise in cytosolic Ca 2+ triggers exocytosis of insulin from secretory vesicles. Type 1 diabetes is characterized by a failure of the immune system that inappropriately recognizes β-cell peptides

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Zhongxiuzi Gao, Li Zhang, Wenting Xie, Siqi Wang, Xiaorui Bao, Yuli Guo, Houjian Zhang, Qingzhong Hu, Yi Chen, Zeen Wang, Maoqiang Xue, and Guanghui Jin

diseased states, including hyperglycemia and DM. Type 1 diabetes arises from autoimmune-induced β-cell damage ( Bluestone et al . 2010 ), whereas type 2 diabetes develops mainly because of insulin resistance ( Kahn et al . 2014 ). Eventually, insulin

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Rijin Xiao, Leah J Hennings, Thomas M Badger, and Frank A Simmen

immune functions ( Yellayi et al. 2002 , Xiao et al. 2005 , Cooke et al. 2006 ). A possible link between Type 1 diabetes, mild or atypical celiac disease, and gastrointestinal lymphoid pathology has been described ( O’Connor et al. 1999 ). Thus