© 2000 Journal of Clinical Pathology
Editorial
The causes and effects of fetal macrosomia in mothers with type 1 diabetes
1 Imperial College School of Medicine, Department of Endocrinology and Metabolic Medicine, Mint Wing, St Mary's Hospital, Praed Street, London W2 1NY, UKstephen.robinson@ic.ac.uk
The mechanisms and physiology of in utero fetal nutrition are not understood, and the proportions of carbohydrate, fat, and protein contributing to fetal energy uptake are unknown. Lipids are energy rich and potentially a valuable source of energy for the fetus. Little intact triglyceride crosses the placenta but non-esterified fatty acids (NEFAs) do cross easily. However, the plasma concentration of maternal NEFAs is too low to sustain the total energy supply to the fetus and, therefore, monosaccharides have been assumed to be the major energy source for the growing fetus.
There are considerable species variations in placental fatty acid transfer. In general, the fewer the numbers of cell layers contributing to the placental barrier the higher the net flux. Most experimental biology of materno–fetal energy transport has been performed in species with non-haemochorial placentation. Human placentation is haemochorial—maternal blood is in direct contact with a thin layer of fetal cells.
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