DNA Methylomes and Epigenetic Age Acceleration Associations with Poor Metabolic Control in T1D.

Biomedicines

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.

Published: December 2020

AI Article Synopsis

  • Type 1 diabetes (T1D) is an autoimmune disease characterized by insulin deficiency and high blood sugar levels, which alters the body's internal environment and forces cells to adapt.
  • The study analyzed DNA methylation patterns in blood samples from 18 T1D patients to identify epigenomic changes related to the disease and metabolic control issues.
  • Over 100 genes showed T1D-related DNA methylation differences, with patients who had poor glycemic control experiencing accelerated epigenetic aging, highlighting the importance of managing the disease for healthy aging.

Article Abstract

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7824441PMC
http://dx.doi.org/10.3390/biomedicines9010013DOI Listing

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