In early pregnancy, the increase in estrogen secretion and insulin levels inhibits lipolysis and promotes the creation of fat stores. Following an initial reduction during the rst eight weeks of pregnancy, plasma levels of triglycerides and cholesterol tend to increase. The high plasma levels of triglycerides seem to be secondary to both an increased hepatic synthesis of VLDL (secondary to the elevation of estrogen levels), as well as a decreased lipoprotein lipase activity (LPL) in the adipose tissue determined by insulin resistance [12, 13].
In the second half of pregnancy, the transition from an anabolic to a catabolic state determines an increase in circulating lipids and promotes its use as an energy source in the mother’s tissues, preserving glucose and amino acids which are transferred toward the fetus [9, 14].
In pregnant women during fasting there is an increase in circulating levels of free fatty acids and ketone compared with a non-pregnant state. Metzger et al. have found that lipid oxidation in pregnant women is highly accelerated with a prompt production of ketone bodies even after a short fast (18 hours) [15]. The typical metabolic changes in response to fasting, that is, plasma glucose and insulin reduction, and plasma free fatty acid and ketone increase, tend to develop much faster in pregnant as opposed to non-pregnant women. Precisely for this reason Freinkel de ned the metabolic fasting pro le of pregnant women as “accelerated starvation” [8].