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Haijiang Wu, Xinna Deng, Yonghong Shi, Ye Su, Jinying Wei, and Huijun Duan

Laakso M 2004 Common polymorphisms of the PPAR-gamma2 (Pro12Ala) and PGC-1alpha (Gly482Ser) genes are associated with the conversion from impaired glucose tolerance to type 2 diabetes in the STOP-NIDDM trial . Diabetologia 47 2176 – 2184

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Gemma Llauradó, Victòria Ceperuelo-Mallafré, Carme Vilardell, Rafael Simó, Pilar Gil, Albert Cano, Joan Vendrell, and José-Miguel González-Clemente

Introduction Cardiovascular disease is the major cause of mortality in type 1 diabetes ( Libby et al . 2005 ). Diabetes mellitus results in an accelerated arteriosclerotic process, which is not fully explained by classical cardiovascular risk

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Anna Krook

Peripheral insulin resistance is characteristic not only for subjects with type 2 diabetes, but a clinically relevant finding also in subjects with type 1 diabetes ( Yki-Järvinen et al . 1987 , Rossetti et al . 1990 , Bingley et al . 2008

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

Introduction Type 1 diabetes is caused by destruction or dysfunction of insulin-producing pancreatic β-cells, and its incidence is increasing in the modern world ( Tuomilehto 2013 ). Protecting β-cells from inflammation and destruction is an

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Chun Zeng, Xin Yi, Danny Zipris, Hongli Liu, Lin Zhang, Qiaoyun Zheng, Krishnamurthy Malathi, Ge Jin, and Aimin Zhou

reduction in insulin-producing pancreatic β-cells has been considered to be one of the key factors in the development of diabetes, particularly type 1 diabetes ( Yoon & Jun 2001 , Mandrup-Poulsen 2003 ). In type 1 diabetes, autoimmune destruction of the

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Rosalia C M Simmen, Dustin M Brown, Charles M Quick, Iad Alhallak, Tyler Rose, Shi J Liu, and Angela S Kelley

Introduction Type 1 diabetes mellitus (T1DM) is an autoimmune disease, resulting from the destruction of insulin-producing β-cells of the pancreatic islets of Langerhans, which leads to a state of hypoinsulinemia and hyperglycemia. In 2015, 1

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Jennifer A Crookshank, Daniel Serrano, Gen-Sheng Wang, Christopher Patrick, Baylie S Morgan, Marie-France Paré, and Fraser W Scott

Introduction Type 1 diabetes (T1D) occurs in a small subset of genetically susceptible individuals whose immune systems destroy most of the pancreatic β-cells. Recent studies suggest that T1D begins in humans at a very early age, but the

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Marika Bogdani, Angela M Henschel, Sanjay Kansra, Jessica M Fuller, Rhonda Geoffrey, Shuang Jia, Mary L Kaldunski, Scott Pavletich, Simon Prosser, Yi-Guang Chen, Åke Lernmark, and Martin J Hessner

Introduction Type 1 diabetes (T1D) is an autoimmune disease characterized by immunocyte infiltration of the pancreatic islets (insulitis) and destruction of the insulin-secreting β cells. Diabetes in the biobreeding (BB) rat exhibits many

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James C Needell, Madalyn N Brown, and Danny Zipris

Introduction Type 1 diabetes (T1D) is a proinflammatory progressive disease thought to be triggered by both genetic and environmental factors ( Atkinson et al . 2014 ). There is evidence supporting the notion that viruses are key players in

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G Üçkaya, P Delagrange, A Chavanieu, G Grassy, M-F Berthault, A Ktorza, E Cerasi, G Leibowitz, and N Kaiser

glucose levels ( Scrocchi et al. 1996 ). GLP-1 and its long-acting analogue exendin 4 were shown to expand the β-cell mass by inducing β-cell proliferation and neogenesis in different animal models of type 2 diabetes ( Xu et al. 1999 ). This effect of