SpringerLink
Log in

Lipid Metabolism in the Human Fetus Development

  • Chapter
  • First Online:
Human Fetal Growth and Development

  • 1981 Accesses

Abstract

Lipids including cholesterol (CHO) and fatty acids (FAs) are main constituents of human body cells and actors in physiological functions thus representing a critical requirement for the embryonic and fetal development.

CHO and FAs attain multiples functions: CHO is a cellular membrane constituent, a steroid hormone, bile acids and oxysterol precursor and it is essential for activation of various signalling pathway (Fielding and Fielding, Biochem Soc Trans 32:65–69, 2004; Cooper et al., Nat Genet 33:508–513, 2003). CHO plays an important role before implantation, as a precursor of progesterone synthesis, and helps in maintaining the early pregnancy (Baardman et al., Biol Reprod 88:1–9, 2013; Murphy, J Reprod Fertil Suppl 55:23–28, 2000; Woollett, Am J Clin Nutr 82:1155–1161, 2005; Herrera et al., Horm Res 65:59–64, 2006; Weissgerber and Wolfe, Appl Physiol Nutr Metab 31:1–11, 2006). When the embryo is implanted in the uterine wall, CHO is determinant for the embryogenesis and morphogenesis and patterning of the central nervous system (Bertrand and Dahmane, Trends Cell Biol 16:597–605, 2006). As well FAs and triglycerides (TGs) are cellular membrane constituents, represent an energy source and take part in neuronal and visual development (Innis, Brain Res 1237:35–43, 2008).

The embrio and fetus do not come in direct contact with the maternal circulation thus are dependent upon tissues surrounding them to receive the nutritional support. These tissues are represented by the yolk sac and trophoblasts, early in the first trimester, then the placenta since the end of the first trimester and the second trimester (Woollett, Am J Clin Nutr 82:1155–1161, 2005). The placenta is an hemochorial villous organ with multiple functions: oxygen and CO2 exchange, nutrient absorbption and immune barrier. It represents a bridge connecting mother and fetus through the maternal-placental (uteroplacental) blood circulation and the fetal-placental (fetoplacental) blood circulation. The functional unit of the placenta is the chorionic villus which contains syncytiotrophoblast/cytotrophoblast, villous stroma and fetal vascular endothelium, layers that separate the maternal blood from the fetal circulation (Wang and Zhao, Vascular biology of the placenta. Morgan & Claypool Life Sciences, San Rafael, 2010). The yolk sac and the placenta provide an adequate nutrient supply by transporting a wide variety of maternal molecules to the embrio and fetus, including lipids, so promoting the intrauterine development. The transfer of some nutrients is regulated by the placenta itself through specific enzymes, receptors and transport proteins; others nutrients are directly metabolized by the placenta.

During gestation metabolic changes intervene with a shift from carbohydrates to lipids for maternal energy production in order to make nutrients available for the fetus (Di Cianni et al., Diabetes Metab Res Rev 19(4):259–70, 2003). Glucose is the main substrate that crosses the placenta but other factors may also contribute to the fetal growth. The fetus requires a substantial amount of lipids throughout its development, the lack of CHO affecting growth disorders (Tint et al., J Pediatr. 127:82–87, 1995). To satisfy these needs maternal physiological hyperlipidemia is manifest in pregnancy; CHO, TGs and FAs concentrations increase in both maternal plasma and erythrocytes thus allowing the fetus to rapidly receive and store fat, which exceeds by far that of any other nutrient (Gil-Sánchez et al., Curr Opin Clin Nutr Metab Care 15:265–272, 2012). Maternal plasma CHO may increase through the 12th week of gestation while TGs reach the 150–300 % of increase in the third trimester of pregnancy (Herrera et al., Horm Res 65:59–64, 2006; Martin et al., Clin Sci 96:421–425, 1999; Amundsen et al., Atherosclerosis 189:451–457, 2006). The two lipoproteins (LPs) classes involved in supporting the placental CHO need are low density lipoprotein (LDL) and high density lipoprotein (HDL) (Tuckey, Placenta 26:273–281, 2005; Henson et al., Endocrinology 137:2067–2074, 1996; Knopp et al., Biol Neonate 50:297–317, 1986). A supply of CHO requirement as a precursor for the production of steroid hormones in the placenta is further critical (Saarelainen et al., Circ J 70:768–777, 2006). Fetal steroid precursors of estrogens regulate the uptake of maternal LPs to promote the placental progesterone synthesis. Both estrogen and progesterone are thus key determinants in pregnancy maintenance and fetal growth so being evident the basic role of fetal and maternal LPs (Pepe and Albrecht, Endocr Rev 16:608–649, 1995; Desoye et al., J Clin Endocrinol Metab 64:704–712, 1987) (Fig. 12.1).

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Log in via an institution

Subscribe and save

Springer+ Basic
EUR 32.99 /Month
  • Get 10 units per month
  • Download Article/Chapter or Ebook
  • 1 Unit = 1 Article or 1 Chapter
  • Cancel anytime
Subscribe now

Buy Now

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 109.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 149.00
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free ship** worldwide - see info
Hardcover Book
USD 149.00
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free ship** worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Similar content being viewed by others

Abbreviations

ABCA1:

ATP-binding cassette A1

ABCG1:

ATP-binding cassette G1

ApoA-1:

Apoprotein A-1

ApoA-4:

Apoprotein A-4

ApoE:

Apoprotein E

CE:

Cholesteryl ester

CETP:

Colesteryl ester transfer protein

CHO:

Cholesterol

HDL:

High density lipoprotein

FA:

Fatty acid

FFA:

Free fatty acid

LCAT:

Lecithin:cholesterol acyl transferase

LDL:

Low density lipoprotein

LP:

Lipoprotein

LRP-1:

LDL-receptor related protein 1

LRP-2:

LDL-receptor related protein 2

NPC1L1:

Niemann-Pick C1-like1

PTP:

Phospholipid transfer protein

SPC-X/2:

Sterol carrier protein X and 2

SR-B1:

Scavenger receptor class B

TG:

Triglyceride

VLDL:

Very low density lipoprotein

References

  1. Fielding CJ, Fielding PE. Membrane cholesterol and the regulation of signal transduction. Biochem Soc Trans. 2004;32:65–9.

    Article  CAS  PubMed  Google Scholar 

  2. Cooper MK, Wassif CA, Krakowiak PA, et al. A defective response to Hedgehog signaling in disorders of cholesterol biosynthesis. Nat Genet. 2003;33:508–13.

    Article  CAS  PubMed  Google Scholar 

  3. Baardman ME, Kerstjens-Frederikse WS, Berger RMF, et al. The role of maternal-fetal cholesterol transport in early fetal life: current insights. Biol Reprod. 2013;88:1–9.

    Article  Google Scholar 

  4. Murphy CR. The plasma membrane transformation of uterine epithelial cells during pregnancy. J Reprod Fertil Suppl. 2000;55:23–8.

    CAS  PubMed  Google Scholar 

  5. Woollett LA. Maternal cholesterol in fetal development: transport of cholesterol from the maternal to the fetal circulation. Am J Clin Nutr. 2005;82:1155–61.

    CAS  PubMed  Google Scholar 

  6. Herrera E, Amusquivar E, Lopez-Soldado I, Ortega H. Maternal lipid metabolism and placental lipid transfer. Horm Res. 2006;65:59–64.

    Article  CAS  PubMed  Google Scholar 

  7. Weissgerber TL, Wolfe LA. Physiological adaptation in early human pregnancy: adaptation to balance maternal-fetal demands. Appl Physiol Nutr Metab. 2006;31:1–11.

    Article  CAS  PubMed  Google Scholar 

  8. Bertrand N, Dahmane N. Sonic Hedgehog signaling in forebrain development and its interactions with pathways that modify its effects. Trends Cell Biol. 2006;16:597–605.

    Article  CAS  PubMed  Google Scholar 

  9. Innis SM. Dietary omega 3 fatty acids and the develo** brain. Brain Res. 2008;1237:35–43.

    Article  CAS  PubMed  Google Scholar 

  10. Wang Y, Zhao S. Vascular biology of the placenta. San Rafael: Morgan & Claypool Life Sciences; 2010.

    Google Scholar 

  11. Di Cianni CG, Miccoli R, Volpe L, et al. Intermediate metabolism in normal pregnancy and in gestational diabetes. Diabetes Metab Res Rev. 2003;19(4):259–70.

    Article  PubMed  Google Scholar 

  12. Tint GS, Salen G, Batta AK, et al. Correlation of severity and outcome with plasma sterol levels in variants of the Smith-Lemli-Opitz syndrome. J Pediatr. 1995;127:82–7.

    Article  CAS  PubMed  Google Scholar 

  13. Gil-Sánchez A, Koletzko B, Larqué E. Current understanding of placental fatty acid transport. Curr Opin Clin Nutr Metab Care. 2012;15:265–72.

    Article  PubMed  Google Scholar 

  14. Martin U, Davies C, Hayavi S, et al. Is normal pregnancy atherogenic? Clin Sci. 1999;96:421–5.

    Article  CAS  PubMed  Google Scholar 

  15. Amundsen AL, Khoury J, Iversen PO, et al. Marked changes in plasma lipids and lipoproteins during pregnancy in women with familial hypercholesterolemia. Atherosclerosis. 2006;189:451–7.

    Article  CAS  PubMed  Google Scholar 

  16. Tuckey RC. Progesterone synthesis by the human placenta. Placenta. 2005;26:273–81.

    Article  CAS  PubMed  Google Scholar 

  17. Henson MC, Shi W, Greene SJ, Reggio BC. Effects of pregnant human, nonpregnant human, and fetal bovine sera on human chorionic gonadotropin, estradiol, and progesterone release by cultured human trophoblast cells. Endocrinology. 1996;137:2067–74.

    CAS  PubMed  Google Scholar 

  18. Knopp RH, Warth MR, Charles D, et al. Lipoprotein metabolism in pregnancy, fat transport to the fetus, and the effects of diabetes. Biol Neonate. 1986;50:297–317.

    Article  CAS  PubMed  Google Scholar 

  19. Saarelainen H, Laitinen T, Raitakari OT, et al. Pregnancy-related hyperlipidemia and endothelial function in healthy women. Circ J. 2006;70:768–77.

    Article  CAS  PubMed  Google Scholar 

  20. Pepe GJ, Albrecht E. Actions of placental and fetal adrenal steroid hormones in primate pregnancy. Endocr Rev. 1995;16:608–49.

    CAS  PubMed  Google Scholar 

  21. Desoye G, Schwenditisch MO, Pfeiffer KP, Zechner R, Kostner GM. Correlation of hormones with lipid and lipoprotein levels during normal pregnancy and postpartum. J Clin Endocrinol Metab. 1987;64:704–12.

    Article  CAS  PubMed  Google Scholar 

  22. Herrera E, Lasunción MA, Gomez-Coronado D, et al. Role of lipoprotein lipase activity on lipoprotein metabolism and the fate of circulating triglycerides in pregnancy. Am J Obstet Gynecol. 1988;158:1575–83.

    Article  CAS  PubMed  Google Scholar 

  23. Jurevics HA, Kidwai FZ, Morell P. Sources of cholesterol during development of the rat fetus and fetal organs. J Lipid Res. 1997;38:723–33.

    CAS  PubMed  Google Scholar 

  24. Avis HJ, Hutten BA, Twickler MT, et al. Pregnancy in women suffering from familial hypercholesterolemia: a harmful period for both mother and newborn? Curr Opin Lipidol. 2009;20:484–90.

    Article  CAS  PubMed  Google Scholar 

  25. Haave NC, Innis SM. Cholesterol synthesis and accretion within various tissues of the fetal and neonatal rat. Metabolism. 2001;50:12–8.

    Article  CAS  PubMed  Google Scholar 

  26. Baardman ME, Erwich JJHM, Berger RMF, et al. The origin of fetal sterols in second-trimester amniotic fluid: endogenous synthesis or maternal-fetal transport? Am J Obstet Gynecol. 2012;207:19–25.

    Article  Google Scholar 

  27. Larque E, Ruiz-Palacios M, Koletzko B. Placental regulation of fetal nutrient supply. Curr Opin Clin Nutr Metab Care. 2013;16:292–7.

    Article  CAS  PubMed  Google Scholar 

  28. Linck LM, Hayflick SJ, Lin DS, et al. Fetal demise with Smith–Lemli–Opitz syndrome confirmed by tissue sterol analysis and the absence of measurable 7-dehydrocholesterol delta(7)-reductase activity in chorionic villi. Prenat Diagn. 2000;20:238–40.

    Article  CAS  PubMed  Google Scholar 

  29. Nowaczyk MJM, Farrell SA, Sirkin WL, et al. Smith–Lemli–Opitz (RHS)syndrome: holoprosencephaly and homozygous IVS8-1G C genotype. Am J Med Genet. 2001;103:75–80.

    Article  CAS  PubMed  Google Scholar 

  30. Parker Jr CR, Deahl T, Drewry P, Hankins G. Analysis of the potential for transfer of lipoprotein-cholesterol across the human placenta. Early Hum Dev. 1983;8:289–95.

    Article  CAS  PubMed  Google Scholar 

  31. Witsch-Baumgartner M, Gruber M, Kraft HG, et al. Maternal apo E genotype is a modifier of the Smith–Lemli–Opitz syndrome. J Med Genet. 2004;41:577–84.

    Article  CAS  PubMed  Google Scholar 

  32. Wadsack C, Hammer A, Levak-Frank S, et al. Selective cholesteryl ester uptake from high density lipoprotein by human first trimester and term villous trophoblast cells. Placenta. 2003;24:131–43.

    Article  CAS  PubMed  Google Scholar 

  33. Descamps OS, Bruniaux M, Guilmot PF, et al. Lipoprotein concentrations in newborns are associated with allelic variations in their mothers. Atherosclerosis. 2004;172:287–98.

    Article  CAS  PubMed  Google Scholar 

  34. Madsen EM, Lindegaard ML, Andersen CB, et al. Human placenta secretes apolipoprotein B-100-containing lipoproteins. J Biol Chem. 2004;279:55271–6.

    Article  CAS  PubMed  Google Scholar 

  35. Wittmaack FM, Gafvels ME, Bronner M, et al. Localization and regulation of the human very low density lipoprotein/apolipoprotein-E receptor: trophoblast expression predicts a role for the receptor in placental lipid transport. Endocrinology. 1995;136:340–8.

    CAS  PubMed  Google Scholar 

  36. Rindler MJ, Traber MG, Esterman AL, et al. Synthesis and secretion of apolipoprotein E by human placenta and choriocarcinoma cell lines. Placenta. 1991;12:615–24.

    Article  CAS  PubMed  Google Scholar 

  37. Lopez D, McLean MP. Estrogen regulation of the scavenger receptor class B gene: anti-atherogenic or steroidogenic, is there a priority? Mol Cell Endocrinol. 2006;247:22–33.

    Article  CAS  PubMed  Google Scholar 

  38. Woollett LA. The origins and roles of cholesterol and fatty acids in the fetus. Curr Opin Lipidol. 2001;12:305–12.

    Article  CAS  PubMed  Google Scholar 

  39. Napoli C, D’Armiento FP, Mancini FP, et al. Fatty streak formation occurs in human fetal aortas and is greatly enhanced by maternal hypercholesterolemia. Intimal accumulation of low density lipoprotein and its oxidation precede monocyte recruitment into early atherosclerotic lesions. J Clin Invest. 1997;100:2680–90.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  40. Woollett LA. Review: transport of maternal cholesterol to the fetal circulation. Placenta. 2011;32 Suppl 2:S218–21.

    Article  PubMed  PubMed Central  Google Scholar 

  41. Ethier-Chiasson M, Duchesne A, Forest JC, et al. Influence of maternal lipid profile on placental protein expression of LDLr and SR-BI. Biochem Biophys Res Commun. 2007;359:8–14.

    Article  CAS  PubMed  Google Scholar 

  42. Lindegaard ML, Wassif CA, Vaisman B, et al. Characterization of placental cholesterol transport: ABCA1 is a potential target for in utero therapy of Smith–Lemli–Opitz syndrome. Hum Mol Genet. 2008;17:3806–13.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. Van Aerde JE, Feldman M, Clandinin MT. Accretion of lipid in the fetus and newborn. In: Polin RA, Fox WW, editors. Fetal and neonatal physiology. 2nd ed. Philadelphia: W. B. Saunders Co; 1998. p. 458–77.

    Google Scholar 

  44. Burt RL, Leake NH, Pulliam RP. Regulation of plasma NEFA in pregnancy and the puerperium. Preliminary observations. Obstet Gynecol. 1961;17:215–21.

    CAS  PubMed  Google Scholar 

  45. Herrera E, Ortega H, Alvino G, et al. Relationship between plasma fatty acid profile and antioxidant vitamins during normal pregnancy. Eur J Clin Nutr. 2004;58:1231–8.

    Article  CAS  PubMed  Google Scholar 

  46. Kitajima M, Oka S, Yasuhi I, et al. Maternal serum triglyceride at 24–32 weeks’ gestation and newborn weight in nondiabetic women with positive diabetic screens. Obstet Gynecol. 2001;97:776–80.

    CAS  PubMed  Google Scholar 

  47. Nolan CJ, Riley SF, Sheedy MT, et al. Maternal serum triglyceride, glucose tolerance, and neonatal birth weight ratio in pregnancy. Diabetes Care. 1995;18:1550–6.

    Article  CAS  PubMed  Google Scholar 

  48. Schaefer-Graf UM, Graf K, Kulbacka I, et al. Maternal lipids as strong determinants of fetal environment and growth in pregnancies with gestational diabetes mellitus. Diabetes Care. 2008;31:1858–63.

    Article  PubMed  PubMed Central  Google Scholar 

  49. Haggarty P. Fatty acid supply to the human fetus. Annu Rev Nutr. 2010;30:237–55.

    Article  CAS  PubMed  Google Scholar 

  50. Catarino C, Rebelo I, Belo L, et al. Fetal lipoprotein changes in pre-eclampsia. Acta Obstet Gynecol Scand. 2008;87:628–34.

    Article  CAS  PubMed  Google Scholar 

  51. Schmid K, Davidson W, Myatt L, Woollett A. Transport of cholesterol across a BeWo cell monolayer: implications for net transport of sterol from maternal to fetal circulation. J Lipid Res. 2003;44:1909–18.

    Article  CAS  PubMed  Google Scholar 

  52. Coleman RA, Haynes EB. Synthesis and release of fatty acids by human trophoblast cells in culture. J Lipid Res. 1987;28:1335–41.

    CAS  PubMed  Google Scholar 

  53. Herrera E, Lasunción MA. Maternal–fetal transfer of lipid metabolites. In: Polin RA, Fox WW, Abman SH, editors. Fetal and neonatal physiology. 3rd ed. Philadelphia: W.B. Saunders Co; 2004. p. 375–88.

    Chapter  Google Scholar 

  54. Herrera E. Lipid metabolism in pregnancy and its consequences in the fetus and newborn. Endocrine. 2002;19:43–55.

    Article  CAS  PubMed  Google Scholar 

  55. Otto SJ, Houwelingen AC, Antal M, Manninen A, et al. Maternal and neonatal essential fatty acid status in phospholipids: an international comparative study. Eur J Clin Nutr. 1997;51:232–42.

    Article  CAS  PubMed  Google Scholar 

  56. Johnsonh Jr J, Simpsonb ER, Carr P, et al. The levels of plasma cholesterol in the human fetus throughout gestation. Pediatr Res. 1982;16:682–3.

    Article  Google Scholar 

  57. Carr BR, Porter JC, Masnald PC, et al. Metabolism of low-density lipoprotein by human fetal adrenal tissue. Endocrinology. 1980;107:1034–340.

    Article  CAS  PubMed  Google Scholar 

  58. Dolphin PJ, Breckenridge WC, Dolphin MA, Tan MH. The lipoproteins of human umbilical cord blood apolipoprotein and lipid levels. Atherosclerosis. 1984;51:109–22.

    Article  CAS  PubMed  Google Scholar 

  59. Averna MR, Barbagallo CM, Di Paola G, et al. Lipids, lipoproteins and apolipoproteins AI, AII, B, CII, CIII and E in newborns. Biol Neonate. 1991;60:187–92.

    Article  CAS  PubMed  Google Scholar 

  60. Parker Jr CR, Carr BR, Simpson ER, MacDonald PC. Decline in the concentration of low-density lipoprotein-cholesterol in human fetal plasma near term. Metabolism. 1983;32:919–23.

    Article  CAS  PubMed  Google Scholar 

  61. Nagasaka H, Chiba H, Kikuta H, et al. Unique character and metabolism of high density lipoprotein (HDL) in fetus. Atherosclerosis. 2002;161:215–23.

    Article  CAS  PubMed  Google Scholar 

  62. Augsten M, Hackl H, Ebner B, et al. Fetal HDL/apoE: a novel regulator of gene expression in human placental endothelial cells. Physiol Genomics. 2011;43:1255–62.

    Article  CAS  PubMed  Google Scholar 

  63. Herz J, Hamann U, Rogne S, et al. Surface location and high affinity for calcium of a 500-kd liver membrane protein closely related to the LDL-receptor suggest a physiological role as lipoprotein receptor. EMBO J. 1998;7:4119–27.

    Google Scholar 

  64. Sreckovic I, Birner-Gruenberger R, Obrist B, et al. Distinct composition of human fetal HDL attenuates its anti-oxidative capacity. Biochim Biophys Acta. 2013;1831:737–46.

    Article  CAS  PubMed  Google Scholar 

  65. Zhao Y, Thorngate FE, Weisgraber KH, et al. Apolipoprotein E is the major physiological activator of lecithin-cholesterol acyltransferase (LCAT) on apolipoprotein B lipoproteins. Biochemistry. 2005;44:1013–25.

    Article  CAS  PubMed  Google Scholar 

  66. Schaefer EJ, Asztalos BF. Increasing high-density lipoprotein cholesterol, inhibition of cholesteryl ester transfer protein, and heart disease risk reduction. Am J Cardiol. 2007;100:25–31.

    Article  Google Scholar 

  67. Scholler M, Wadsack C, Metso J, et al. Phospholipid transfer protein is differentially expressed in human arterial and venous placental endothelial cells and enhances cholesterol efflux to fetal HDL. J Clin Endocrinol Metab. 2012;97:2466–74.

    Article  CAS  PubMed  Google Scholar 

  68. Duttaroy AK. Transport of fatty acids across the human placenta: a review. Prog Lipid Res. 2009;48:52–61.

    Article  CAS  PubMed  Google Scholar 

  69. Haggarty P. Placental regulation of fatty acid delivery and its effect on fetal growth-a review. Placenta. 2002;23:S28–38.

    Article  PubMed  Google Scholar 

  70. Hanebutt FL, Demmeimair H, Schiessl B, et al. Long-chain polyunsaturated fatty acid (LC-PUFA) transfer across the placenta. Clin Nutr. 2008;27:685–93.

    Article  CAS  PubMed  Google Scholar 

  71. Mahley RW, Huang Y. Apolipoprotein E: from atherosclerosis to Alzheimer’s disease and beyond. Curr Opin Lipidol. 1999;10:207–17.

    Article  CAS  PubMed  Google Scholar 

  72. Descamps OS, Bruniaux M, Guilmot PF, et al. Lipoprotein metabolism of pregnant women is associated with both their genetic polymorphisms and those of their newborn children. J Lipid Res. 2005;46:2405–14.

    Article  CAS  PubMed  Google Scholar 

  73. Potter JM, Nestel PJ. The hyperlipidemia of pregnancy in normal and complicated pregnancies. Am J Obstet Gynecol. 1979;133:165–70.

    Article  CAS  PubMed  Google Scholar 

  74. Vuorio AF, Miettinen TA, Turtola H, et al. Cholesterol metabolism in normal and heterozygous familial hypercholesterolemic newborns. J Lab Clin Med. 2002;140:35–42.

    Article  CAS  PubMed  Google Scholar 

  75. Toleikyte I, Retterstøl K, Leren TP, et al. Pregnancy outcomes in familial hypercholesterolemia: a registry-based study. Circulation. 2011;124:1606–14.

    Article  PubMed  Google Scholar 

  76. Khoury J, Amundsen AL, Tonstad S, et al. Evidence for impaired physiological decrease in the uteroplacental vascular resistance in pregnant women with familial hypercholesterolemia. Acta Obstet Gynecol Scand. 2008;29:1–5.

    Google Scholar 

  77. van der Graaf A, Vissers MN, Gaudet D, et al. The dyslipidemia of mothers with familial hypercholesterolemia deteriorates lipid levels in their adult offspring. Boston: Oral presentation at the International Atherosclerosis Society Conference; 2010.

    Google Scholar 

  78. Serdar Z, Gur E, Colakodullary’ M, et al. Lipid and protein oxidation and antioxidant function in women with mild and severe preeclampsia. Arch Gynecol Obstet. 2003;268:19–25.

    CAS  PubMed  Google Scholar 

  79. Var A, Kuscu N, Koyuncu F, et al. Atherogenic profile in preeclampsia. Arch Gynecol Obstet. 2003;268:45–7.

    CAS  PubMed  Google Scholar 

  80. Belo L, Caslake M, Gaffney D, et al. Changes in LDL size and HDL concentration in normal and preeclamptic pregnancies. Atherosclerosis. 2002;162:425–32.

    Article  CAS  PubMed  Google Scholar 

  81. Rodie V, Caslake M, Stewart F, et al. Fetal cord plasma lipoprotein status in uncomplicated human pregnancies complicated. Atherosclerosis. 2004;176:181–7.

    Article  CAS  PubMed  Google Scholar 

  82. Murata M, Kodama H, Goto K, et al. Decreased very-low-density lipoprotein and low-density lipoprotein receptor messenger ribonucleic acid expression in placentas from preeclamptic pregnancies. Am J Obstet Gynecol. 1996;175:1551–6.

    Article  CAS  PubMed  Google Scholar 

  83. Tabano S, Alvino G, Antonazzo P. Placental LPL gene expression is increased in severe intrauterine growth-restricted pregnancies. Pediatr Res. 2006;59:250–3.

    Article  CAS  PubMed  Google Scholar 

  84. DeRuiter MC, Alkemade FE, Gittenberger-de Groot AC, et al. Maternal transmission of risk for atherosclerosis. Curr Opin Lipidol. 2008;19:333–7.

    Article  CAS  PubMed  Google Scholar 

  85. Herrera E, Ortega-Senovilla H. Disturbances in lipid metabolism in diabetic pregnancy – are these the cause of the problem? Best Pract Res Clin Endocrinol Metab. 2010;24:515–25.

    Article  CAS  PubMed  Google Scholar 

  86. Herrera E, Ortega-Senovilla H. Lipid metabolism during pregnancy and its implications for fetal growth. Curr Pharm Biotechnol. 2014;15:24–31.

    Article  CAS  PubMed  Google Scholar 

  87. Sattar N, Greer IA, Galloway PJ, et al. Lipid and lipoprotein concentrations in pregnancies complicated by intrauterine growth restriction. J Clin Endocrinol Metab. 1999;84:128–30.

    CAS  PubMed  Google Scholar 

  88. Pecks U, Brieger M, Schiessl B, et al. Maternal and fetal cord blood lipids in intrauterine growth restriction. J Perinat Med. 2012;40:287–96.

    Article  CAS  PubMed  Google Scholar 

  89. Porter FD. Smith–Lemli–Opitz syndrome: pathogenesis, diagnosis and management. Eur J Hum Genet. 2008;16:535–54.

    Article  CAS  PubMed  Google Scholar 

  90. Goldenberg A, Wolf A, Chevy F, et al. Antenatal manifestations of Smith-Lemli-Opitz (RSH) syndrome: a retrospective survey of 30 cases. Am J Med Genet A. 2004;124:423–6.

    Article  Google Scholar 

  91. Quelin C, Loget P, Verloes A, et al. Phenotypic spectrum of fetal Smith-Lemli-Opitz syndrome. Eur J Med Genet. 2012;55:81–90.

    Article  PubMed  Google Scholar 

  92. Irons M, Elias ER, Salen G, et al. Defective cholesterol biosynthesis in Smith-Lemli-Opitz syndrome. Lancet. 1993;341:1414.

    Article  CAS  PubMed  Google Scholar 

  93. Nowaczyk MJ, Irons MB. Smith-Lemli-Opitz syndrome: phenotype, natural history, and epidemiology. Am J Med Genet C: Semin Med Genet. 2012;15:250–62.

    Article  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Department of Health Science and Pediatrics, Turin University, Piazza Polonia, 94, Torino, 10126, Italy

    Ornella Guardamagna MD & Paola Cagliero PhD

Authors
  1. Ornella Guardamagna MD
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Paola Cagliero PhD
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Ornella Guardamagna MD .

Editor information

Editors and Affiliations

  1. Calcutta School of Tropical Medicine, Kolkata, India

    Niranjan Bhattacharya

  2. Boston University, Jamaica Plain, Massachusetts, USA

    Phillip G. Stubblefield

Rights and permissions

Reprints and permissions

Copyright information

© 2016 Springer International Publishing Switzerland

About this chapter

Cite this chapter

Guardamagna, O., Cagliero, P. (2016). Lipid Metabolism in the Human Fetus Development. In: Bhattacharya, N., Stubblefield, P. (eds) Human Fetal Growth and Development. Springer, Cham. https://doi.org/10.1007/978-3-319-14874-8_12

Download citation

  • DOI: https://doi.org/10.1007/978-3-319-14874-8_12

  • Published:

  • Publisher Name: Springer, Cham

  • Print ISBN: 978-3-319-14873-1

  • Online ISBN: 978-3-319-14874-8

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics

Search

Navigation