Maternal obesity disrupts folate metabolism

According to the Linus Pauling Institute at Oregon State University, folate (which includes folates from food and folic acid supplements) is important for amino acid metabolism and methylation reactions in the body. Anyone who has had a baby knows that folic acid is an important nutrient to prevent the birth defect spina bifida. Folate and vitamin B-12 deficiency may also lead to a type of anemia known as megaloblastic anemia.

Spina Bifida (Open Defect) Diagram Image from CDC

New research published in Physiological Reports examined baboons to find out how maternal obesity and excess nutrient availability to the fetus influenced their risk for developing health problems as adults. They were specifically interested in maternal and fetal regulation of methionine, which is important for normal development. Methyl-micronutrients can be obtained from maternal ingestion of such nutrients as folate, choline, betaine as well as vitamin B-12.

Mothers who were fed a diet high in fat and energy both prior to as well as throughout gestation delivered offspring that had 16% lower weight than those delivered by normal weight mothers. Moreover, the offspring of baboons with maternal obesity had impaired folate metabolism because the mothers were deficient in vitamin B-12. In addition, fetal concentrations of methionine, glycine, serine and taurine were also lower.

The findings of this study show that the methionine cycle is disrupted with maternal obesity and this disruption may lead to epigenetic changes in the offspring. This is relevant to primates, including humans, as it offers both a diagnostic opportunity for pregnancies in which the mother is obese as well as treatment opportunities should methionine dysregulation be discovered.


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