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Restriction of maternal dietary carbohydrate decreases fetal brain indoles and glycogen in rats
K G Koski1, L Lanoue, S N Young
1School of Dietetics and Human Nutrition, Macdonald Campus of McGill University, Ste. Anne de Bellevue, Québec, Canada.
In spite of evidence that dietary carbohydrate can increase brain tryptophan and 5-hydroxytryptamine in adult rats, the possible influence of maternal dietary carbohydrate on fetal brain indoles has received little attention. We studied the effect of graded levels (0, 4, 12 and 60%) of maternal dietary fructose or glucose fed throughout pregnancy on fetal brain glycogen and indoles. The diets were isoenergetic and met the NRC energy requirements for pregnant rats. The results demonstrated that low maternal dietary carbohydrate, with adequate energy intake, reduced fetal brain weight and concentrations of glycogen, tryptophan, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid. There were no significant differences between glucose and fructose feeding at any dietary carbohydrate level for any fetal brain measurements, showing that it was the level and not the type of dietary carbohydrate that was important. Significant correlations between fetal brain 5-hydroxytryptamine and brain glycogen, and between fetal brain 5-hydroxytryptamine and brain weight, suggested that lowered brain 5-hydroxytryptamine was only one symptom of disrupted brain development in fetuses of dams fed low levels of carbohydrate. The results show that dietary carbohydrate restriction during pregnancy can have adverse effects on fetal brain development, glycogen levels, and neurotransmitter synthesis even when maternal dietary protein and energy intake are adequate.
In spite of evidence that dietary carbohydrate can increase brain tryptophan and 5-hydroxytryptamine in adult rats, the possible influence of maternal dietary carbohydrate on fetal brain indoles has received little attention. We studied the effect of graded levels (0, 4, 12 and 60%) of maternal dietary fructose or glucose fed throughout pregnancy on fetal brain glycogen and indoles. The diets were isoenergetic and met the NRC energy requirements for pregnant rats. The results demonstrated that low maternal dietary carbohydrate, with adequate energy intake, reduced fetal brain weight and concentrations of glycogen, tryptophan, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid. There were no significant differences between glucose and fructose feeding at any dietary carbohydrate level for any fetal brain measurements, showing that it was the level and not the type of dietary carbohydrate that was important. Significant correlations between fetal brain 5-hydroxytryptamine and brain glycogen, and between fetal brain 5-hydroxytryptamine and brain weight, suggested that lowered brain 5-hydroxytryptamine was only one symptom of disrupted brain development in fetuses of dams fed low levels of carbohydrate. The results show that dietary carbohydrate restriction during pregnancy can have adverse effects on fetal brain development, glycogen levels, and neurotransmitter synthesis even when maternal dietary protein and energy intake are adequate.