In Utero One-Carbon Metabolism Interplay and Metabolic Syndrome in Cardiovascular Disease Risk Reduction

Abstract

The maternal obesogenic environment plays a role in programing the susceptibility of the fetus to postnatal non-alcoholic fatty liver disease (NAFLD), a risk factor for cardiovascular disease (CVD). NAFLD is a multisystem disease that is characterized by hepatic fat accumulation due in part to dysregulated energy metabolism network through epigenetic mechanisms such as DNA methylation. DNA methylation affects fetal programing and disease risk via regulation of gene transcription; it is affected by methyl donor nutrients such as vitamin B₁₂ , methionine, folic acid, vitamin B₆ , and choline. Although several studies have documented the role of several maternal methyl donor nutrients on obesity-induced NAFLD in offspring, currently, data are lacking on its impact on CVD risk as an endpoint. The aim of this paper is to use current knowledge to construct a postulation for the potential role of a comprehensive gestational methyl donor nutrients supplementary approach on the susceptibility of offspring to developing metabolic-syndrome-related cardiovascular complications.

Keywords: DNA methylation; cardiovascular disease; fetal programming; maternal one-carbon metabolism; non-alcoholic fatty liver disease.