In cases where the increased demand for nutrients during pregnancy is not met by the diet alone the shortfall may be made up from the maternal stores and the placenta may play a role in orchestrating some of the maternal nutritional adaptations in pregnancy. For example, placentally derived leptin is a potent stimulator of lipolysis and there is evidence that the rate of export into the maternal circulation is controlled to allow the placenta to modulate its own substrate supply in response to the fetal demand for fats. The various homeostatic mechanisms within the placenta and their interaction with maternal physiological adaptations during pregnancy act to ensure a constant supply of substrate to the fetus, free of large diurnal fluctuations corresponding to the timing of maternal meals, and to protect the fetus against a transiently poor intake during critical periods of fetal growth. These adaptations help the mother to meet the full fetal requirement for nutrients such as LCPUFA and iron whilst consuming apparently poor diets.
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