Role of lipoprotein lipase activity on lipoprotein metabolism and the fate of circulating triglycerides in pregnancy

Herrera, Emílio; Lasunción, Miguel A.; Gómez-Coronado, Diego; Aranda, Pilar; López-Luna, Pilar; Maier, Isabel

doi:10.1016/0002-9378(88)90193-7

Cited by 183 publications

(143 citation statements)

References 37 publications

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“…Total maternal lipoprotein lipase activity is reduced in women in late pregnancy and animal models indicate a redistribution of the available activity towards the placenta and away from adipose tissue and liver (Herrera et al, 1988). Thus, it is likely that the dietary lipid is preferentially available to the placenta.…”

Section: Implications For Dietary Recommendationsmentioning

confidence: 99%

Effect of placental function on fatty acid requirements during pregnancy

Haggarty¹

2004

Eur J Clin Nutr

187

156

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The fetus has an absolute requirement for the n-3/n-6 fatty acids and docosahexaenoic acid (22:6 n-3; DHA) in particular is essential for the development of the brain and retina. Most of the fat deposition in the fetus occurs in the last 10 weeks of pregnancy. The likely rate of DHA utilisation during late pregnancy cannot be met from dietary sources alone in a significant proportion of mothers. De novo synthesis makes up some of the shortfall but the available evidence suggests that the maternal adipose tissue makes a significant contribution to placental transport to the fetus. The placenta plays a crucial role in mobilising the maternal adipose tissue and actively concentrating and channelling the important n-3/n-6 fatty acids to the fetus via multiple mechanisms including selective uptake by the syncytiotrophoblast, intracellular metabolic channelling, and selective export to the fetal circulation. These mechanisms protect the fetus against low long-chain polyunsaturated fatty acid (LCPUFA) intakes in the last trimester of pregnancy and have the effect of reducing the maternal dietary requirement for preformed DHA at this time. As a result of these adaptations, small changes in the composition of the habitual maternal diet before pregnancy are likely to be more effective in improving LCPUFA delivery to the fetus than large dietary changes in late pregnancy. There is little evidence that DHA intake/status in the second half of pregnancy affects visual and cognitive function in the offspring, but more studies are needed, particularly in children born to vegetarian and vegan and mothers who may have very low intakes of DHA.

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Section: Implications For Dietary Recommendationsmentioning

confidence: 99%

Effect of placental function on fatty acid requirements during pregnancy

Haggarty¹

2004

Eur J Clin Nutr

187

156

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“…Maternal circulating triglycerides (TGs) and FFAs are increased during the third trimester, providing a source of FFAs for milk production, placental uptake, and possibly transfer to the fetus (10). A gestational increase in estrogen, which stimulates the production of VLDLs, together with a decreased removal of lipoprotein TGs by LPL and/or hepatic lipase, has been suggested to be responsible for this hyperlipidemia (11).…”

mentioning

confidence: 99%

Gestational and hormonal regulation of human placental lipoprotein lipase

Magnusson-Olsson

Hamark

Ericsson

et al. 2006

Journal of Lipid Research

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The fetal demand for FFA increases as gestation proceeds, and LPL represents one potential mechanism for increasing placental lipid transport. We examined LPL activity and protein expression in first trimester and term human placenta. The LPL activity was 3-fold higher in term (n 5 7; P , 0.05) compared with first trimester (n 5 6) placentas. The LPL expression appeared lower in microvillous membrane from first trimester (n 5 2) compared with term (n 5 2) placentas. We incubated isolated placental villous fragments with a variety of effectors [GW 1929, estradiol, insulin, cortisol, epinephrine, insulin-like growth factor-1 (IGF-1), and tumor necrosis factor-a] for 1, 3, and 24 h to investigate potential regulatory mechanisms. Decreased LPL activity was observed after 24 h of incubation with estradiol (1 mg/ml), insulin, cortisol, and IGF-1 (n 5 12; P , 0.05). We observed an increase in LPL activity after 3 h of incubation with estradiol (20 ng/ml) or hyperglycemic medium plus insulin (n 5 7; P , 0.05).

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“…In vitro cultures of tissue homogenates or cellular components of human placenta have previously demonstrated the ability of this tissue to lipolyze triglyceride-rich lipoproteins (3,8,9,12,13). However, it has not been possible in humans to show that this activity is directed toward the maternal compartment as in animals (28,29). In our study, we present the first in vivo argument for such orientation of placental LPL activity.…”

Section: Discussionmentioning

confidence: 63%

Lipoprotein metabolism of pregnant women is associated with both their genetic polymorphisms and those of their newborn children

Descamps

Bruniaux

Guilmot

et al. 2005

Journal of Lipid Research

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To explore whether the placenta contributes to the lipoprotein metabolism of pregnant women, we took advantage of the fact that placental proteins are encoded from the fetal genome and examined the associations between lipids of 525 pregnant women and the presence, in their newborns, of genetic polymorphisms of LPL and apolipoprotein E (APOE), two genes expressed in placenta. After adjustment for maternal polymorphisms, newborn LPL*S447X was associated with lower triglycerides ( ؊ 21 ؎ 9 mg/dl), lower LDL-cholesterol (LDL-C; ؊ 12 ؎ 5 mg/dl), lower apoB ( ؊ 14 ؎ 4 mg/dl), higher HDL-C (5 ؎ 2 mg/dl), and higher apoA-I (9 ؎ 4 mg/dl) in their mothers; newborn LPL*N291S was associated with higher maternal triglycerides (114 ؎ 31 mg/dl); and newborn APOE*E2 (compared to E3E3) was associated with higher maternal LDL-C (14 ؎ 6 mg/dl) and higher maternal apoB (14 ؎ 5 mg/dl). These associations (all P Ͻ 0.05) were independent of polymorphisms carried by the mothers and of lipid concentrations in newborns and were similar in amplitude to the associations between maternal polymorphisms and maternal lipids.Such findings support the active role of placental LPL and APOE in the metabolism of maternal lipoproteins and suggest that fetal genes may modulate the risk for problems related to maternal dyslipidemia (preeclampsia, pancreatitis, and future cardiovascular disease). -Descamps, O. S., M. Bruniaux, P-F. Guilmot, R. Tonglet, and F. R.

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Role of lipoprotein lipase activity on lipoprotein metabolism and the fate of circulating triglycerides in pregnancy

Cited by 183 publications

References 37 publications

Effect of placental function on fatty acid requirements during pregnancy

Effect of placental function on fatty acid requirements during pregnancy

Gestational and hormonal regulation of human placental lipoprotein lipase

Lipoprotein metabolism of pregnant women is associated with both their genetic polymorphisms and those of their newborn children

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