Abstract
Choline, or its metabolites, is required for maintaining the structural integrity and signaling function of cell membranes, for providing a pool of methyl-groups available for the methylation of biological molecules, and for cholinergic neurotransmission. This nutrient is also necessary for the export of lipids from the liver and for normal muscle cell function. Choline can be synthesized de novo in the liver, but this pathway alone does not meet human requirements for this nutrient and, therefore, choline must be derived from the diet. Symptoms of choline deficiency in humans include fat accumulation in the liver as well as liver and muscle cell damage. The developing fetus has a high demand for choline that is met by supply from the mother across the placenta. The amount of choline available to the fetus during pregnancy can have significant effects on its brain development; women with the lowest choline intake during pregnancy are more likely to have babies with neural tube defects. Animals born to mothers who were perinatally supplemented with choline show enhanced memory function, which persists throughout life without further dietary choline supplementation. In rodents, maternal dietary choline during pregnancy influences proliferation, apoptosis, migration, and differentiation of neuronal precursor cells in fetal hippocampus. These effects of choline may be mediated by epigenetic mechanisms.
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