Purpose of Review
Post-prandial lipemia (PPL), characterized by elevated levels of triglyceride (TG) following a meal, is an independent risk factor for cardiovascular disease. This review summarizes current knowledge on the genetic and epigenetic determinants of the PPL TG response and provides perspectives on future directions.
Recent Findings
Recent studies suggested that PPL-related traits have heritability between 38 and 80%. Genomics studies identified genetic variants in or near APOA1/C3/A4/A5 cluster region affecting PPL TG levels. Epigenomics studies found DNA methylation levels of many genes known to be related to lipid metabolism including CPT1A gene are associated with fasting TG and PPL TG.
Summary
Both genetic polymorphisms and epigenetic modifications are important determinants of PPL variation. Epigenetics may have even more significant impact than genetic variants on PPL. Further studies with multi-omics system biology approach are needed to fully elucidate the mechanisms of PPL regulation to combat the atherogenic effect of PPL.