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Concentrations of choline and phosphocholine in the fetal brain of the laboratory rat are unaffected by maternal diets deficient in folic acid, choline or methionine

Published online by Cambridge University Press:  30 August 2013

W. D. Rees
Affiliation:
University of Aberdeen, Rowett Institute of Health and Nutrition, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
S. M. Hay
Affiliation:
University of Aberdeen, Rowett Institute of Health and Nutrition, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK
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Abstract

Type
Abstract
Copyright
Copyright © The Authors 2013 

Studies have shown that giving choline supplements to pregnant animals leads to impressive improvements in the cognitive ability of the offspring throughout their entire lifespan and may protect them against the adverse effects of ageing( Reference Meck, Williams, Cermak and Blusztajn 1 Reference Meck and Williams3 ). Current evidence from human trials also suggests that there is an improvement in cognitive function in the offspring of mothers who eat more choline( Reference Wu, Dyer, King, Richardson and Innis 4 , Reference Boeke, Gillman, Hughes, Rifas-Shiman, Villamor and Oken5 ). The ways in which choline helps the fetal brain develop are not fully established, but it is known to improve the growth of specific brain regions( Reference Craciunescu, Albright, Mar, Song and Zeisel 6 ) possibly by contributing to the synthesis of cell membranes via phosphocholine. The metabolism of choline is closely linked to that of folic acid and methionine and it is possible that maternal diets deficient in any one of these components may impact on the availability of choline or phosphocholine in the fetal brain. The aim of the present study was to measure choline and phosphocholine concentrations in the fetal brain of rats fed B vitamin deficient diets.

Pregnant rats were fed one of five experimental diets; complete diet (Control), deficient in folic acid (-F), deficient in folic acid and low in choline (-F LC), deficient in folic acid and low in methionine (-F LM) or one deficient in all three key methyl donors, folic acid, choline and methionine (-F LM LC) and for comparison one group of animals were fed the stock diet (Stock)( Reference Maloney, Hay and Rees 7 ). Animals were killed on d21 of gestation and the fetal brains were harvested. Choline and phosphocholine concentrations were measured as described previously( Reference Maloney, Hay and Rees 7 ). Data were analysed by ANOVA.

Concentrations of both free choline and phosphocholine in the fetal brain were unaffected by the provision of folic acid, methionine or choline in the maternal diet. Previously we have shown that the phosphocholine content of the maternal liver was reduced by about 20% in the dams fed these low choline experimental diets, and when combined with a low methionine diet, phosphocholine concentrations were reduced by approximately 60%( Reference Maloney, Hay and Rees 7 ). Conversely folate deficient diets increased free choline in the maternal liver by approximately two fold ( Reference Maloney, Hay and Rees 7 ). Despite these marked changes in maternal choline metabolism there were no changes in the concentrations of either choline or phosphocholine in the fetal brain. This study suggests that the benefits of choline supplementation on neural development may be an indirect consequence of improved maternal metabolism.

References

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