The levels of triglyceride, free and ester cholesterol, and phospholipids were studied in peanut oil-cholesterol diet fed nondiabetic and alloxan-diabetic pregnant rabbits and their fetuses. The relative percentage of fatty acid composition was also determined in the cholesterol ester, triglyceride, nonesterified fatty acid, and phospholipid fractions of the maternal and fetal plasma lipids.

In 2 groups of pregnant rabbits, one fed a stock diet and the other fed a peanut oil-cholesterol diet, the maternal and fetal plasma levels of phospholipids, triglycerides, ester and free cholesterol were determined. The relative percentage of fatty acid composition of the phospholipid, nonesterified fatty acid, triglyceride and cholesterol ester fractions were also studied. The changes in maternal plasma lipid levels and fatty acid composition correlated well with the amount of fat and the fatty acid composition of the diets consumed by the 2 groups. The only significant change in the level of these plasma lipids in the fetus of the 2 groups was a small increase in the cholesterol ester level of the fat-cholesterol diet group. There were several alterations in the fatty acid composition of the fetal plasma lipids between the two dietary groups. Nearly one half of these were correlated with changes in the diets consumed by the maternal rabbits. Changes in fetal plasma fatty acid composition that correlated with the diets consumed were at least partly explained on a placental transport basis. The changes in fetal fatty acid composition that were not correlated with the diet were probably due to indirect dietary-induced changes in fetal lipid metabolism, possibly through multiple step pathways.

Phospholipid, triglyceride, cholesterol ester, and free cholesterol levels were determined in the serum of normal and alloxan diabetic maternal rabbits and their fetuses. The only significant difference between the level of serum lipid in the two groups was a decrease in fetal free cholesterol in the alloxan diabetic group. The decrease in fetal free cholesterol is apparently due to either decreased synthesis or increased degradation of free cholesterol by the fetus since it is unlikely that it can cross the placental barrier.