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