Journal
PHYSIOLOGICAL GENOMICS
Volume 50, Issue 11, Pages 947-955Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physiolgenomics.00072.2018
Keywords
cardiovascular disease; chromatin; epigenetics; histone modifications; metabolic syndrome; methylation; non-coding RNA; obesity; Type II diabetes
Categories
Funding
- Washington University Department of Genetics
- Diabetes Research Center at Washington University [P30DK-020579]
- National Institutes of Health [K01 DK-095003, T32 GM-007067]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [K01DK095003, P30DK020579] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007067] Funding Source: NIH RePORTER
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The dramatic increase in global prevalence of metabolic disease is inexplicable when considering only environmental or only genetic factors, leading to the need to explore the possible roles of epigenetic factors. A great deal of progress has been made in this interdisciplinary field in recent years, with many studies investigating various aspects of the metabolic syndrome and its associated epigenetic changes. Rodent models of metabolic diseases have been particularly illuminating because of the ability to leverage tools such as genetic and environmental modifications. The current review summarizes recent breakthroughs regarding epigenetic markers in studies of obesity, Type II diabetes, and cardiovascular disease, the three major disorders associated with metabolic syndrome. We also discuss open questions and future directions for integrating genomic, epigenomic, and phenotypic big biodata toward understanding metabolic syndrome etiology.
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