Abstract
ABSTRACTSupplementation with myo-inositol during the periconceptional period of pregnancy may ameliorate the recurrence risk of having a fetus affected by a neural tube defect (NTD; e.g., spina bifida). This could be of particular importance in providing a means for preventing NTDs that are unresponsive to folic acid. This review highlights the characteristics of inositol and describes the role of myo-inositol in the prevention of NTDs in rodent studies and the evidence for its efficacy in reducing NTD risk in human pregnancy. The possible reduction in NTD risk by maternal myo-inositol implies functional and developmentally important maternal–embryonic inositol interrelationships and also suggests that embryonic uptake of myo-inositol is crucial for embryonic development. The establishment of active myo-inositol cellular uptake mechanisms in the embryonic stages of human pregnancy, when the neural tube is closing, is likely to be an important determinant of normal development. We draw attention to the generation of materno-fetal inositol concentration gradients and relationships, and outline a transport pathway by which myo-inositol may be delivered to the early developing human embryo. These considerations provide novel insights into the mechanisms that may underpin inositol's ability to confer embryonic developmental benefit.
Highlights
Inositol is present in a variety of foods including nuts, seeds, vegetables and fruit, with myo-inositol (Figure 1) being the predominant isomeric form [1]
In the first trimester of pregnancy, the coelomic fluid that bathes the yolk sac, an organ of maternal–embryonic nutrient exchange, contains high concentrations of inositol and other polyols. These likely derive from maternal plasma that percolates from the maternal spiral arteries and/or from uterine decidual gland secretions, together with potential synthesis by the placenta and embryo/fetus
This indicates that the polyol metabolic pathway in the human conceptus is highly active in the early weeks of pregnancy to maintain ATP concentrations and cellular redox potential while the embryo develops in a low oxygen environment
Summary
Stephen W D’Souza, Andrew J Copp, Nicholas DE Greene, and Jocelyn D Glazier3 1Maternal and Fetal Health Research Centre, St. Mary’s Hospital, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom; 2Newlife Birth Defects Research Centre, Developmental Biology and Cancer Department, UCL Great Ormond Street Institute of Child Health, London, United Kingdom; and 3Division of Evolution and Genomic Sciences, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom
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