Accumulating evidence suggest a role for epigenetic mechanisms as well as gene–environment interactions in the development of metabolic and endocrine disorders. Epigenetic alterations have been reported in type 2 Diabetes, obesity, and metabolic syndrome, where environmental and lifestyle factors are potentially important influences that contribute to disease pathogenesis via interacting with the genome and inducing epigenetic changes.
We are inviting original research articles, methods articles, and reviews which address the role of epigenetic regulation in metabolic and endocrine related disorders including:
· Epigenome-wide association studies.
· Studies integrating epigenetic and genetic information as well as integrative analysis of multi-omics datasets.
· Studies identifying epigenetic biomarkers for early disease prediction or for predicting response to therapy.
· Studies describing epigenetic programming during fetal in-utero development and susceptibility to metabolic diseases during later adult life.
Accumulating evidence suggest a role for epigenetic mechanisms as well as gene–environment interactions in the development of metabolic and endocrine disorders. Epigenetic alterations have been reported in type 2 Diabetes, obesity, and metabolic syndrome, where environmental and lifestyle factors are potentially important influences that contribute to disease pathogenesis via interacting with the genome and inducing epigenetic changes.
We are inviting original research articles, methods articles, and reviews which address the role of epigenetic regulation in metabolic and endocrine related disorders including:
· Epigenome-wide association studies.
· Studies integrating epigenetic and genetic information as well as integrative analysis of multi-omics datasets.
· Studies identifying epigenetic biomarkers for early disease prediction or for predicting response to therapy.
· Studies describing epigenetic programming during fetal in-utero development and susceptibility to metabolic diseases during later adult life.