Epigenetics, broadly defined as a heritable change in genomic output that does not involve changes in DNA sequence, serves to mediate the influence of the environment on the genome. Epigenetic control of gene expression involves multiple regulatory mocules, such as DNA methylation, histone modifications, 3D chromatin architecture, and non coding RNAs. The incidence of both type 1 and type 2 diabetes has increased over the past half-century at a rate that cannot be explained by genetic factors alone. In addition, our lifestyle has undergone significant changes in this timespan. While multiple genes associated with diabetes have been identified, they account for only a fraction of hereditary diabetes cases. Altogether, this points to the contribution of gene-environment interactions and epigenetics, to the development of metabolic diseases. Multiple studies show that parental over- and under-nutrition increase the risk of metabolic syndrome in parent as well as the offspring. This has spurred significant interest in understanding the role of epigenetic programming in health and glucose homeostasis throughout the lifespan. Genome-wide profiling of DNA methylation and histone modifications has further advanced our understanding of how patterning of the epigenome shapes a cell’s identity, and its response to the environment in health and diabetes.
The aim of this Research Topic is to review recent and noteworthy work on the epigenetic regulation of glucose homeostasis in health, and how epigenetic dysregulation contributes the pathogenesis of diabetes and its many complications. While recent work has unequivocally established the contribution of epigenetic factors in the development and inheritance of diabetes risk, the precise mechanisms are still far from clear. It is not completely understood how the different epigenetic regulatory modules interact with each other to dictate the cellular phenotype. In addition, the links between environmental and lifestyle factors, nutrition, metabolism, and the epigenome are only now beginning to emerge. Therefore, this Research Topic aims to provide a platform to comprehensively cover the recent advances in the field and highlight how epigenetic mechanisms contribute to glucose homeostasis and whether this can be leveraged for therapeutic purposes in diabetes.
The following subtopics will be covered in this Research Topic:
• Epigenetic regulation in metabolic tissues such as islets, liver, muscle, adipose.
o Different epigenetic regulatory modules and how they interact with each other.
• Epigenetic dysregulation in the pathogenesis and complications of diabetes.
• The epigenome and GWAS studies.
• Epigenetic regulation in fetal and neonatal life, and implications for future risk of metabolic disease.
o Epigenetic control of tissue differentiation etc.
o Imprinting control
o The effect of parental nutritional status on the offspring
o The effect of external factors (environment, stress etc) during development on the pathogenesis of metabolic disease in adulthood.
• The interaction between nutrient sensing, metabolism, and the epigenome.
o The contribution of circadian clock and other environmental factors, such as diet.
• Emerging directions in epigenetic biomarkers and therapeutics.
This Research Topic welcomes only review or mini review articles on the above subtopics.
Epigenetics, broadly defined as a heritable change in genomic output that does not involve changes in DNA sequence, serves to mediate the influence of the environment on the genome. Epigenetic control of gene expression involves multiple regulatory mocules, such as DNA methylation, histone modifications, 3D chromatin architecture, and non coding RNAs. The incidence of both type 1 and type 2 diabetes has increased over the past half-century at a rate that cannot be explained by genetic factors alone. In addition, our lifestyle has undergone significant changes in this timespan. While multiple genes associated with diabetes have been identified, they account for only a fraction of hereditary diabetes cases. Altogether, this points to the contribution of gene-environment interactions and epigenetics, to the development of metabolic diseases. Multiple studies show that parental over- and under-nutrition increase the risk of metabolic syndrome in parent as well as the offspring. This has spurred significant interest in understanding the role of epigenetic programming in health and glucose homeostasis throughout the lifespan. Genome-wide profiling of DNA methylation and histone modifications has further advanced our understanding of how patterning of the epigenome shapes a cell’s identity, and its response to the environment in health and diabetes.
The aim of this Research Topic is to review recent and noteworthy work on the epigenetic regulation of glucose homeostasis in health, and how epigenetic dysregulation contributes the pathogenesis of diabetes and its many complications. While recent work has unequivocally established the contribution of epigenetic factors in the development and inheritance of diabetes risk, the precise mechanisms are still far from clear. It is not completely understood how the different epigenetic regulatory modules interact with each other to dictate the cellular phenotype. In addition, the links between environmental and lifestyle factors, nutrition, metabolism, and the epigenome are only now beginning to emerge. Therefore, this Research Topic aims to provide a platform to comprehensively cover the recent advances in the field and highlight how epigenetic mechanisms contribute to glucose homeostasis and whether this can be leveraged for therapeutic purposes in diabetes.
The following subtopics will be covered in this Research Topic:
• Epigenetic regulation in metabolic tissues such as islets, liver, muscle, adipose.
o Different epigenetic regulatory modules and how they interact with each other.
• Epigenetic dysregulation in the pathogenesis and complications of diabetes.
• The epigenome and GWAS studies.
• Epigenetic regulation in fetal and neonatal life, and implications for future risk of metabolic disease.
o Epigenetic control of tissue differentiation etc.
o Imprinting control
o The effect of parental nutritional status on the offspring
o The effect of external factors (environment, stress etc) during development on the pathogenesis of metabolic disease in adulthood.
• The interaction between nutrient sensing, metabolism, and the epigenome.
o The contribution of circadian clock and other environmental factors, such as diet.
• Emerging directions in epigenetic biomarkers and therapeutics.
This Research Topic welcomes only review or mini review articles on the above subtopics.
