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Abstract
The fetus has a high requirement for cholesterol and synthesizes cholesterol at elevated rates. Recent studies suggest that fetal cholesterol also can be obtained from exogenous sources. The purpose of the current study was to examine the transport of maternal cholesterol to the fetus and determine the mechanism responsible for any cholesterol-driven changes in transport. Studies were completed in pregnant hamsters with normal and elevated plasma cholesterol concentrations. Cholesterol feeding resulted in a 3.1-fold increase in the amount of LDL-cholesterol taken up by the fetus and a 2.4-fold increase in the amount of HDL-cholesterol taken up. LDL-cholesterol was transported to the fetus primarily by the placenta, and HDL-cholesterol was transported by the yolk sac and placenta. Several proteins associated with sterol transport and efflux, including those induced by activated liver X receptor, were expressed in hamster and human placentas: NPC1, NPC1L1, ABCA2, SCP-x, and ABCG1, but not ABCG8. NPC1L1 was the only protein increased in hypercholesterolemic placentas. Thus, increasing maternal lipoprotein-cholesterol concentrations can enhance transport of maternal cholesterol to the fetus, leading to 1) increased movement of cholesterol down a concentration gradient in the placenta, 2) increased lipoprotein secretion from the yolk sac (shown previously), and possibly 3) increased placental NPC1L1 expression.
Highlights
The fetus has a high requirement for cholesterol and synthesizes cholesterol at elevated rates
Any maternally derived lipoprotein-cholesterol that is in the fetus would have been taken up first by the placenta and/or yolk sac, transported across the trophoblasts and visceral endoderm cells of the placenta and yolk sac, respectively, and effluxed and/or secreted into the fetal circulation
fractional catabolic rate (FCR) was defined as pools of LDL- or HDL-cholesterol cleared from plasma/time per gram of tissue or whole tissue by the placenta, yolk sac, and fetus of normo- and hypercholesterolemic dams
Summary
The fetus has a high requirement for cholesterol and synthesizes cholesterol at elevated rates. LDL-cholesterol was transported to the fetus primarily by the placenta, and HDL-cholesterol was transported by the yolk sac and placenta. Increasing maternal lipoprotein-cholesterol concentrations can enhance transport of maternal cholesterol to the fetus, leading to 1) increased movement of cholesterol down a concentration gradient in the placenta, 2) increased lipoprotein secretion from the yolk sac (shown previously), and possibly 3) increased placental NPC1L1 expression.—Burke, K. Maternal plasma triglyceride and cholesterol concentrations increase during pregnancy in humans [3, 4], possibly an adaptation to maternal and fetal needs. Whether these changes in maternal lipoprotein concentrations result in increased transport of maternal cholesterol to the fetus is unclear. These studies were supported by grants HD34089 (LAW) and GM31651 (FS) from the NIH and 053025N from the AHA (GAG)
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