One carbon metabolism and early development: a diet-dependent destiny

Abstract

One carbon metabolism (OCM) is critical for early development, as it provides one carbon (1C) units for the biosynthesis of DNA, proteins, and lipids and epigenetic modification of the genome. Epigenetic marks established early in life can be maintained and exert lasting impacts on gene expression and functions later in life. Animal and human studies have increasingly demonstrated that prenatal 1C nutrient deficiencies impair fetal growth, neurodevelopment, and cardiometabolic parameters in childhood, while sufficient maternal 1C nutrient intake is protective against these detrimental outcomes. However, recent studies also highlight the potential risk of maternal 1C nutrient excess or imbalance in disrupting early development. Further studies are needed to delineate the dose-response relationship among prenatal 1C nutrient exposure, epigenetic modifications, and developmental outcomes.

Keywords: early development; epigenetics; fetal programming; methyl donor; one carbon metabolism.