Maternal and fetal cord blood lipids in intrauterine growth restriction

Pecks, Ulrich; Brieger, Meike; Schießl, Barbara; Bauerschlag, Dirk; Piroth, Daniela; Bruno, Benjamin; Fitzner, C.; Orlikowsky, Thorsten; Maass, Nicolaì; Rath, Werner

doi:10.1515/jpm.2011.135

Cited by 78 publications

(79 citation statements)

References 30 publications

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“…In our study, we observed that in serum HDL-Cholesterol in IUGR group was lower than those in a term AGA group, which was a statistically significant finding.This finding is similar with study conducted by Pecks U et al 19 Maternal cholesterol is actively transferred via the placenta. At the apical placental surface facing maternal blood, i.e., the syncytiotrophoblast, many lipoprotein receptors are involved in cholesterol uptake.…”

Section: Serum Hdl-cholesterolsupporting

confidence: 93%

“…before the 6th month) fetal LDL correlates to LDL levels of the mothers, while in third trimester this correlation is virtually absent. 19 From above observation and from our study observation we can say that a basal LDL production rate is maintained by the fetus throughout gestation. Throughout pregnancy maternal LDL may contribute to the fetal LDL pool with decreasing amounts, until at term the LDL concentration reflects the basal production rate of the fetus.…”

Section: Serum Ldl-cholesterolsupporting

confidence: 64%

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Atherogenic lipid profile of intrauterine growth retarded newborns

et al. 2016

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Section: Serum Hdl-cholesterolsupporting

confidence: 93%

Section: Serum Ldl-cholesterolsupporting

confidence: 64%

Atherogenic lipid profile of intrauterine growth retarded newborns

et al. 2016

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“…Conversely, increased TGs during pregnancy have been shown to augment the risk of preeclampsia, preterm birth, and fetal growth restriction (FGR) ( 2,5 ). The lipid metabolism and plasma levels are also affected by maternal factors such as body mass index (BMI), maternal weight gain, maternal nutrition, prepregnancy lipid levels, and various medical complications of pregnancy such as diabetes ( 6 ).…”

Section: Rna Extraction and Cdna Synthesismentioning

confidence: 99%

Is the atherosclerotic phenotype of preeclamptic placentas due to altered lipoprotein concentrations and placental lipoprotein receptors? Role of a small-for-gestational-age phenotype

Hentschke

Poli-de-Figueiredo

Costa

et al. 2013

Journal of Lipid Research

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Gestational hyperlipidemia is a common factor in pregnancy in which the maternal circulating lipid profile changes from an anabolic to a catabolic state, increasing lipids, especially triglycerides (TGs) and lipoproteins ( 1 ). From the 12th week of gestation, phospholipids, total cholesterol (TC), LDL, HDL, and TGs increase in response to estrogen stimulation and insulin resistance ( 2 ). Thus, during the fi rst two trimesters, it is common to see maternal fat accumulation; however, in the third trimester there is enhanced lipolytic activity and decreased lipoprotein lipase (LPL) activity in the adipose tissue, consequently, fat storage declines or ceases ( 3 ). Early in gestation, the lipids are required to develop the fetal brain and central nervous system ( 4 ), to build cell membranes, and as a precursor of bile acids and steroid hormones ( 2 ). However, a maternal source of lipids is still required until term, but in lower amounts, possibly due to some fetal-derived lipids Abstract Atherosis of spiral arteries in uteroplacental beds from preeclamptic women resemble those of atherosclerosis, characterized by increased plasma lipids and lipoproteins. We hypothesized that: 1 ) lipoprotein receptors/ transporters in the placenta would be upregulated in preeclampsia, associated with increased maternal and fetal lipoprotein concentrations; and 2 ) expression of these would be reduced in preeclamptic placentae from women delivering small-for-gestational-age (SGA) infants. Placental biopsies and maternal and umbilical serum samples were taken from 27 normotensive and 24 preeclamptic women. Maternal/ umbilical cord serum LDL, HDL, total cholesterol, and triglycerides were measured. Placental mRNA expression of lipoprotein receptors/transporters were quantifi ed using quantitative RT-PCR. Protein localization/expression of LDL receptor-related protein 1 (LRP-1) in the preeclamptic placentae with/without SGA was measured by immunohistochemistry. Placental mRNA expression of all genes except paraoxonase-1 ( PON-1 ), microsomal triglyceride transfer protein ( MTTP ), and protein disulfi de isomerase family A member 2 ( PDIA2 ) were observed. No differences for any lipoprotein receptors/transporters were found between groups; however, in the preeclamptic group placental LRP-1 expression was lower in SGA delivering mothers (n = 7; P = 0.036). LRP-1 protein was localized around fetal vessels and Hofbauer cells. This is the fi rst detailed study of maternal/fetal lipoprotein concentrations and placental lipoprotein receptor mRNA expression in normotensive and preeclamptic pregnancies. These fi ndings do not support a role of altered lipid metabolism in preeclampsia, but may be involved in fetal growth. -Hentschke, M. R., C. E. Abbreviations: AGA, adequate-for-gestational-age; BMI, body mass index; FGR, fetal growth restriction; FGR-M, fetal growth restriction without hemodynamic changes; FGR-S, fetal growth restriction with hemodynamic changes; IQR, interquartile range; LDL-R , LDL receptor; LRP-1, LDL receptor-related pro...

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“…There is increasing evidence shown that an abnormal lipid profile during gestation may increase the risk of cardiovascular disease and result in undesirable outcomes for the mother and the fetus, including preeclampsia [7,8], gestational diabetes mellitus [9,10], intrauterine growth restriction and premature birth [11,12].…”

Section: Introductionmentioning

confidence: 99%