The relationship between maternal glycemia and macrosomia

Fetal glucose availability is a direct function of maternal glucose levels, since glucose is transported across the placenta to the conceptus by facilitated diffusion. The normal fetus has a relatively immature system for controlling its own blood glucose levels. Thus, although present in the fetal circulation from the earliest stages of pregnancy, plasma levels of insulin and glucagon are relatively fixed in the fetus and appear to be adapted to the narrow physiologic range of glucose seen in the normal fetus. Thus, the fetal pancreatic beta-cell is stimulated by physiologic levels of neither glucose nor amino acids, nor is it inhibited by fetal hypoglycemia. Likewise, the fetal pancreatic alpha-cell is relatively unresponsive to stimuli, so that fetal hyperglycemia does not lower fetal glucagon levels nor does fetal hyperaminoacidemia stimulate them. Accordingly, the normal human fetus can be considered a passive recipient of glucose from the mother. To the extent that the maternal adaptive responses are adequate, the fetus will not experience high-amplitude perturbations in its own blood glucose levels.