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Review Article

Normalizing Metabolism in Diabetic Pregnancy: Is It Time to Target Lipids?

  1. Helen L. Barrett1,2,3⇑,
  2. Marloes Dekker Nitert1,3,
  3. H. David McIntyre3,4 and
  4. Leonie K. Callaway2,3
  1. 1UQ Centre for Clinical Research, The University of Queensland, Herston, Queensland, Australia
  2. 2Obstetric Medicine, Royal Brisbane and Women’s Hospital, Herston, Queensland, Australia
  3. 3School of Medicine, The University of Queensland, St. Lucia, Queensland, Australia
  4. 4Mater Medical Research Institute, Queensland, Australia
  1. Corresponding author: Helen L. Barrett, h.barrett{at}uq.edu.au.
Diabetes Care 2014 May; 37(5): 1484-1493. https://doi.org/10.2337/dc13-1934
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    Maternal lipoprotein metabolism in late pregnancy. In the last trimester, elevated maternal insulin resistance and estrogen levels produce multiple changes in lipoprotein metabolism. These include a reduction of LPL activity in adipose tissue and serum, a reduction in hepatic lipase (HL), and an enhancement of the activity of cholesterol ester transfer protein (CETP). These alterations result in increased adipose tissue lipolysis, increasing the release of free fatty acids (FFAs) and glycerol from adipose tissue and their transfer to the liver and placenta. These substrates are used in the liver for gluconeogenesis, VLDL production, and ketone body synthesis and by the placenta. The VLDL produced in the liver has a higher triglyceride concentration than in the nonpregnant population. CETP activity transfers triglycerides from VLDL to LDL and HDL. HDL2b increases more than the other HDL subfractions, due to a decrease in hepatic lipase activity and increased lecithin-cholesterol acyltransferase (LCAT) activity. In the fasting state, hepatic gluconeogenesis and hepatic β-oxidation are greatly increased, resulting in ketone body synthesis, providing potential alternative maternal fuel supplies and maintaining other substrate loads for fetal utilization. The mammary gland has increased LPL activity in late gestation and lactation. FFAs, cholesterol, glucose, ketone bodies, and amino acids can all be metabolized in the placenta. *Exaggerated in diabetic pregnancy. +See Fig. 2. This figure has been based in part on Herrera and Ortega-Senovilla (3). AA, amino acid; IR, insulin resistance; TG, triglyceride.

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    Proposed mechanisms involved in fatty acid and cholesterol transfer across the placenta. Maternal free fatty acids (FFAs) can be directly taken up into the trophoblast. Lipases, in particular endothelial lipase and LPL, release FFA from the maternal circulating lipoproteins (58). The placenta also takes up cholesterol. This is used in placental steroid hormone synthesis as well as transported to the fetus. The trophoblast expresses receptors for VLDL cholesterol (VLDL receptor), LDL-C (LDL receptor), and HDL-C (scavenger receptor class B type 1 [SR-B1]). After uptake, the cholesterol ester is hydrolyzed by the lysosome/endosome pathway (59). The mechanisms for release of FFAs and cholesterol from the fetal side of the syncytiotrophoblast and fetal endothelial cells are less well defined than those for uptake from the maternal side. FFAs move to the fetal circulation by facilitated diffusion or using fatty acid translocase (FAT/CD36) and fatty acid transport protein (FATP) in the syncytiotrophoblast basal membrane. Cholesterol is moved out of the trophoblast by secretion of lipoproteins, through complex formation with apoE, and efflux by SR-B1, ABCA1, and ABCG1 (59). Direct uptake of chylomicron remnant particles has been demonstrated in mouse placenta, raising the possibility that this may also occur in human pregnancy (9). This figure has been adapted from references 3,8,9,58–60. FABPpm, plasma membrane fatty acid binding protein; LR, lipoprotein receptor; LRP, lipoprotein-related protein; SR-A, scavenger receptor A.

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Diabetes Care: 37 (5)

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May 2014, 37(5)
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Normalizing Metabolism in Diabetic Pregnancy: Is It Time to Target Lipids?
Helen L. Barrett, Marloes Dekker Nitert, H. David McIntyre, Leonie K. Callaway
Diabetes Care May 2014, 37 (5) 1484-1493; DOI: 10.2337/dc13-1934

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Normalizing Metabolism in Diabetic Pregnancy: Is It Time to Target Lipids?
Helen L. Barrett, Marloes Dekker Nitert, H. David McIntyre, Leonie K. Callaway
Diabetes Care May 2014, 37 (5) 1484-1493; DOI: 10.2337/dc13-1934
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    • Introduction
    • Lipid Metabolism in Pregnancy
    • Maternal Lipids in Diabetic Pregnancy
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