DNA Methylomes and Epigenetic Age Acceleration Associations with Poor Metabolic Control in T1D
Raúl F Pérez,
Juan Luis Fernandez-Morera,
Judit Romano-Garcia,
Edelmiro Menendez-Torre,
Elias Delgado-Alvarez,
Mario F Fraga,
Agustin F Fernandez
Affiliations
Raúl F Pérez
Nanomaterials and Nanotechnology Research Center (CINN-CSIC), Health Research Institute of Asturias (ISPA), Institute of Oncology of Asturias (IUOPA), and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), 33011 Oviedo, Asturias, Spain
Juan Luis Fernandez-Morera
Nanomaterials and Nanotechnology Research Center (CINN-CSIC), Health Research Institute of Asturias (ISPA), Institute of Oncology of Asturias (IUOPA), and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), 33011 Oviedo, Asturias, Spain
Judit Romano-Garcia
Servicio de Anestesiologia y Reanimacion, Hospital Universitario Central de Asturias (HUCA), 33011 Oviedo, Asturias, Spain
Edelmiro Menendez-Torre
Endocrinology and Nutrition Department, Hospital Universitario Central de Asturias (HUCA), 33011 Oviedo, Asturias, Spain
Elias Delgado-Alvarez
Endocrinology and Nutrition Department, Hospital Universitario Central de Asturias (HUCA), 33011 Oviedo, Asturias, Spain
Mario F Fraga
Nanomaterials and Nanotechnology Research Center (CINN-CSIC), Health Research Institute of Asturias (ISPA), Institute of Oncology of Asturias (IUOPA), and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), 33011 Oviedo, Asturias, Spain
Agustin F Fernandez
Nanomaterials and Nanotechnology Research Center (CINN-CSIC), Health Research Institute of Asturias (ISPA), Institute of Oncology of Asturias (IUOPA), and Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), 33011 Oviedo, Asturias, Spain
Type 1 diabetes (T1D) is an autoimmune disease that leads to insulin deficiency and hyperglycemia. Little is known about how this metabolic dysfunction, which substantially alters the internal environment, forces cells to adapt through epigenetic mechanisms. Consequently, the purpose of this work was to study what changes occur in the epigenome of T1D patients after the onset of disease and in the context of poor metabolic control. We performed a genome-wide analysis of DNA methylation patterns in blood samples from 18 T1D patients with varying levels of metabolic control. We identified T1D-associated DNA methylation differences on more than 100 genes when compared with healthy controls. Interestingly, only T1D patients displaying poor glycemic control showed epigenetic age acceleration compared to healthy controls. The epigenetic alterations identified in this work make a valuable contribution to improving our understanding of T1D and to ensuring the appropriate management of the disease in relation to maintaining healthy aging.
