title: DNA methylation as a diagnostic and therapeutic target in the battle against Type 2 diabetes.
abstract: Type 2 diabetes (T2D) develops due to insulin resistance and impaired insulin secretion, predominantly in genetically predisposed subjects exposed to nongenetic risk factors like obesity, physical inactivity and ageing. Emerging data suggest that epigenetics also play a key role in the pathogenesis of T2D. Genome-wide studies have identified altered DNA methylation patterns in pancreatic islets, skeletal muscle and adipose tissue from subjects with T2D compared with nondiabetic controls. Environmental factors known to affect T2D, including obesity, exercise and diet, have also been found to alter the human epigenome. Additionally, ageing and the intrauterine environment are associated with differential DNA methylation. Together, these data highlight a key role for epigenetics and particularly DNA methylation in the growing incidence of T2D.
authors.affiliation: Epigenetics & Diabetes, Department of Clinical Sciences in Malmö, Lund University Diabetes Centre, Lund University, CRC, Jan Waldenströms gata 35, 205 02 Malmö, Sweden.
authors.forename: Tina
authors.initials: T
authors.lastname: Rönn
authors.affiliation: Epigenetics & Diabetes, Department of Clinical Sciences in Malmö, Lund University Diabetes Centre, Lund University, CRC, Jan Waldenströms gata 35, 205 02 Malmö, Sweden.
authors.forename: Charlotte
authors.initials: C
authors.lastname: Ling
mesh_terms: D019175:DNA Methylation; D003924:Diabetes Mellitus, Type 2 / Q000175:diagnosis / Q000235:genetics* / Q000628:therapy; D044127:Epigenesis, Genetic; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000235:genetics; D000078790:Insulin Secretion
chemical_list: D007328:Insulin
keywords: BMI; CpG-SNPs; HbA1c; adipose tissue; epigenetics; exercise; insulin resistance; insulin secretion; pancreatic islets; skeletal muscle