[Pre-beta-migrating lipoprotein A-I concentration in normal full-term maternal blood]

Hyperlipidemia in pregnancy accompanying selectively-raised concentrations of serum apolipoprotein A-I (apoA-I) and high-density lipoprotein-2-cholesterol (HDL2-C) had been considered to be, at least in part, mediated by sex hormones. On the other hand, it is known that oral estrogen-replacement therapies in postmenopausal women raise serum concentrations of lipoprotein A-I without apoA-II (LpA-I) originated from the liver. This study was performed to clarify the relations among the concentrations of pre-beta-migrating LpA-I (pre-betaLpA-I) and of serum apoA-I and of HDL-C. And we discussed the origin of pre-beta LpA-I in normal full-term maternal blood. Pre-beta LpA-I concentrations in 12 maternal (mean +/- SD = 33.8 +/- 7.6 mg/dl) and umbilical cord blood (mean +/- SD = 3.1 +/- 1.9 mg/dl) pairs and those in 20 healthy non-pregnant adult female controls (mean +/- SD = 13.5 +/- 6.1 mg/dl) were determined using the crossed immunoelectrophoresis. (1) The higher concentration of maternal pre-beta LpA-I than that of control was contributed to the high concentration of maternal serum apoA-I but not to the high concentration of maternal HDL-C, so it would loosen the correlativity between serum apoA-I concentration and HDL-C concentration because pre-beta LpA-I was cholesterol-poor. (2) It did not correlate with the high concentration of chylomicron, which made us speculate that maternal pre-betaLpA-I might be possible to be originated from the liver by the action of endogenous estrogen. And, (3) no correlation between the concentrations of pre-beta LpA-I from maternal blood and those from cord blood respectively will support the idea that their lipoprotein metabolisms would be independent with each other.