differences between groups, but by 16 and 18 hours, the pregnant women had substantial increases in free fatty acid (FFA) and β-hydroxybutyrate (βHA), both of which were inversely correlated with glucose levels. There was a significant difference in FFA concentrations between obese and lean pregnant women only at 16 hours of fasting. In contrast, there were no significant differences in βHA levels at any time point between lean and obese women.
As first described by Freinkel (1980), pregnancy can be considered a condition of “accelerated starvation” because of the changes in maternal metabolism that occur because of the increase in insulin resistance. As discussed previously, the accelerated starvation occurs as a result of increased insulin resistance, particularly related to lipid metabolism. There is an increased risk of developing ketonuria and ketonemia in pregnancy even among women with normal glucose tolerance. Chez and Curcio (1987) reported that eight of nine women with clinically normal pregnancies developed ketonuria at various times during their pregnancy. Using a portable capillary meter, Gin et al. (2006) measured capillary blood ketones and βHA in women with normal glucose tolerance (controls) and those with GDM three times a day from 25 to 37 weeks’ gestation. Fasting ketonuria was strongly correlated with ketonemia in controls but not in women with GDM. There was a chronic increase in ketonemia levels in 12 percent of the controls and 47 percent of the women with GDM.
Pregnant women develop ketonemia much earlier than nonpregnant women during prolonged fasting because of the accelerated starvation. Felig (1973) studied women between 16 and 22 weeks’ gestation who elected termination of pregnancy and were willing to undergo prolonged fasting and compared them with a nonpregnant control group. After an overnight fast of at least 12 hours and for the first 36 to 60 hours of starvation, blood βHA and acetoacetate concentrations were two- to threefold higher in the pregnant group than in the nonpregnant group. The increase in lipolysis among the pregnant women was attributed to increases in hPL. The ketone concentrations in maternal blood were equivalent to those in amniotic fluid and were fortyfold above levels in fed subjects. The assumption is that amniotic fluid levels represent maternal-to-fetal transport. Felig (1973) also hypothesized that ketones become an important metabolic fuel for the fetal brain once glucose concentrations decrease, because the human fetal brain has the enzymes necessary for ketone oxidation.
Coetzee et al. (1980) reported that 19 percent of obese, insulin-dependent diabetic women on 1,000-kilocalorie (kcal) diets developed ketonuria. In contrast, in diabetic women eating higher-energy diets, only 14 percent had