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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

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

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

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

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

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

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

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

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

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