Biomedical Updates


Choline Deficiency Affects Fetal Memory Development

Fetal progenitor cells multiply, migrate, differentiate and undergo apoptosis at different yet specific times during fetal development. An investigation at the University of North Carolina at Chapel Hill, NC studied the need for choline by these cells for membrane synthesis and for methylation.1

Choline is increasingly thought to modulate epigenetic regulation of gene expression in both neuronal and endothelial progenitor cells, thereby modifying brain development. Accordingly, these mechanisms explain why, in mice and rat models, maternal dietary intake of choline influences both angiogenesis and neurogenesis in fetal hippocampus, and results in life-long changes in memory function.

This also may explain why women eating diets low in choline have a greater risk of having a baby with a birth defect. Choline is mainly found in foods that contain fat and cholesterol, and intake of such foods has diminished in response to dietary advice from nutritionists and physicians. As little as 2 generations ago, diets commonly contained choline-rich foods but today U.S. women tend to eat diets low in choline content.

Premenopausal women normally may require less choline in their diet than do men and postmenopausal women, because estrogen induces the gene for the enzyme catalyzing endogenous biosynthesis of the choline-containing phospholipid phosphatidylcholine.

However, many women have a single nucleotide polymorphism (SNP) that blocks the induction of endogenous biosynthesis, thereby making them require more dietary choline. When these women eat diets low in choline, the supply of this nutrient to the fetus is likely to be inadequate, and may perturb progenitor cell proliferation, migration, differentiation, and apoptosis.

Reference

  1. Zeisel SH. The supply of choline is important for fetal progenitor cells. Semin Cell Dev Biol 2011 Jun 12. [Epub ahead of print]

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