Maternal Hyperlipidemia in Pregnancy

Salameh, Wael A.; Mastrogiannis, Dimitrios

doi:10.1097/00003081-199403000-00011

Cited by 57 publications

(37 citation statements)

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“…But others reported that triglycerides progressively increased throughout pregnancy and that cholesterol concentrations fell during the first 8-12 wk of gestation and then rose linearly until parturition (3,35). Increased cholesterol levels are thought to reflect increased production of sex steroids (9,52), whereas increased triglycerides may relate to the nutritional requirements of the mother and fetus (9,52 (31), or increased thyroid activity (51,57). Cholesterol levels are known to be inversely related to thyroid function (26), although in pregnant women, increased cholesterol levels and increased thyroid function have been reported to occur (7).…”

Section: Methodsmentioning

confidence: 99%

Changes in Clinical Pathology Parameters During Gestation in the New Zealand White Rabbit

et al. 1999

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Hematology and serum chemistry parameters were analyzed in 2 groups of pregnant rabbits to assess changes in these parameters over the course of gestation. These data were used to generate a historical control reference range for embryofetal development regulatory toxicology studies. During the 28-day gestation period, the following major changes were observed. Red blood cell counts, hemoglobin, and hematocrit increased slightly up to day 13

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Section: Methodsmentioning

confidence: 99%

Changes in Clinical Pathology Parameters During Gestation in the New Zealand White Rabbit

et al. 1999

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“…Cholesterol is obtained endogenously by de novo synthesis and exogenously by transfer of maternal cholesterol to the fetus. Interestingly, maternal plasma triglyceride and cholesterol concentrations increase during pregnancy in humans (3,4), possibly an adaptation to maternal and fetal needs. However, whether these changes in maternal lipoprotein concentrations result in increased transport of maternal cholesterol to the fetus is unclear.…”

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confidence: 99%

Transport of maternal cholesterol to the fetus is affected by maternal plasma cholesterol concentrations in the Golden Syrian hamster

Burke

Colvin

Myatt

et al. 2009

Journal of Lipid Research

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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 possi- Cholesterol is essential for normal fetal development. Possibly the most noted role of cholesterol is as a structural component of membranes. Sterols are also the precursor for bile acids, steroid hormones, and oxysterols, which are all synthesized by the fetus and regulate various cellular processes. Cholesterol is also required for activation of sonic hedgehog (Shh), a protein involved in brain development, and for propagation of the Shh signal (1, 2). Cholesterol is obtained endogenously by de novo synthesis and exogenously by transfer of maternal cholesterol to the fetus. Interestingly, maternal plasma triglyceride and cholesterol concentrations increase during pregnancy in humans (3, 4), possibly an adaptation to maternal and fetal needs. However, whether these changes in maternal lipoprotein concentrations result in increased transport of maternal cholesterol to the fetus is unclear.Since the fetus does not come in direct contact with the maternal circulation, maternal cholesterol destined for the fetus must initially be taken up by the placenta and yolk sac prior to transport and delivery to the fetus. Indeed, the placenta and yolk sac take up maternal LDL-and HDLcholesterol at relatively elevated rates compared with other peripheral tissues (5). LDL is taken up by the LDL receptor (LDLR), which is expressed abundantly in the placenta but expressed at low levels, if at all, in the yolk sac (5, 6). LDL-derived sterol is transported to the lysosome/endosome pathway where the ester bond is hydrolyzed (7). The unesterified cholesterol is then transported by NiemannThese studies were supported by grants HD34089 (LAW) and GM31651 (FS) from the...

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“…The decreases in expression of RXRs, PPARs, LXRs, FXR, TRs, SREBPs, and PGC-1s could contribute to the alterations in lipid metabolism during late pregnancy. farnesoid X receptor; liver X receptor; peroxisome proliferator-activated receptor; retinoid X receptor; lipid metabolism IN MANY ANIMALS, INCLUDING HUMANS, there is an increase in serum triglyceride and cholesterol levels during the third trimester of pregnancy because of an increase in circulating VLDL and LDL (16,17,46). A number of factors contribute to this increase in circulating lipids (16 -18).…”

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confidence: 99%

Decreased nuclear hormone receptor expression in the livers of mice in late pregnancy

Sweeney

Moser²,

Shigenaga³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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During the third trimester of pregnancy, there is an increase in serum triglyceride and cholesterol levels. The mechanisms accounting for these changes in lipid metabolism during pregnancy are unknown. We hypothesized that, during pregnancy, the expression of nuclear hormone receptors involved in regulating lipid metabolism would decrease. In 19-day pregnant mice, serum triglyceride and non-HDL cholesterol levels were significantly increased, whereas total cholesterol was slightly decreased, because of a decrease in the HDL fraction. Peroxisome proliferator-activated receptor (PPAR)␣, PPAR␤/␦, and PPAR␥, liver X receptor (LXR)␣ and LXR␤, farnesoid X receptor (FXR), and retinoid X receptor (RXR)␣, RXR␤, and RXR␥ mRNA levels were significantly decreased in the livers of 19-day pregnant mice. Additionally, the expressions of thyroid receptor (TR)␣, pregnane X receptor, sterol regulatory element-binding proteins (SREBP)-1a, SREBP-1c, SREBP-2, and liver receptor homolog 1 were also decreased, whereas the expression of TR␤, constitutive androstane receptor, and hepatic nuclear factor 4 showed no significant change. mRNA levels of the PPAR target genes carnitine-palmitoyl transferase 1␣ and acyl-CoA oxidase, the LXR target genes SREBP1c, ATP-binding cassettes G5 and G8, the FXR target gene SHP, and the TR target genes malic enzyme and Spot14 were all significantly decreased. Finally, the expressions of PPAR␥ coactivator (PGC)-1␣ and PGC-1␤, known activators of a number of nuclear hormone receptors, were also significantly decreased. The decreases in expression of RXRs, PPARs, LXRs, FXR, TRs, SREBPs, and PGC-1s could contribute to the alterations in lipid metabolism during late pregnancy. farnesoid X receptor; liver X receptor; peroxisome proliferator-activated receptor; retinoid X receptor; lipid metabolism IN MANY ANIMALS, INCLUDING HUMANS, there is an increase in serum triglyceride and cholesterol levels during the third trimester of pregnancy because of an increase in circulating VLDL and LDL (16,17,46). A number of factors contribute to this increase in circulating lipids (16 -18). Adipose tissue lipoprotein lipase activity is reduced (18), leading to a decrease in the clearance of triglyceride-rich lipoproteins. Moreover, triglyceride synthesis is decreased in adipose tissue, whereas lipolysis is enhanced during pregnancy (18), resulting in an increase in serum free fatty acid levels. In the liver, pregnancy leads to a reduction in fatty acid oxidation (15), although fatty acid synthesis is increased (62). The increase in de novo fatty acid synthesis and the enhanced delivery of fatty acids from adipose tissue coupled with the decrease in fatty acid oxidation increase the pool of fatty acids available in the liver, resulting in an increase in triglyceride synthesis (58). The activity of diacylglycerol acetyltransferase, a key enzyme in the synthesis of triglycerides, is also increased in the liver during pregnancy (50). This increase in triglyceride synthesis in the liver leads to an increase in the hepatic produc...

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Maternal Hyperlipidemia in Pregnancy

Cited by 57 publications

References 0 publications

Changes in Clinical Pathology Parameters During Gestation in the New Zealand White Rabbit

Changes in Clinical Pathology Parameters During Gestation in the New Zealand White Rabbit

Transport of maternal cholesterol to the fetus is affected by maternal plasma cholesterol concentrations in the Golden Syrian hamster

Decreased nuclear hormone receptor expression in the livers of mice in late pregnancy

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