Lipid Metabolism in Pregnancy

Herrera, Emílio; Gómez-Coronado, Diego; Lasunción, Miguel A.

doi:10.1159/000242635

Cited by 84 publications

(66 citation statements)

References 197 publications

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“…To be transported to the fetal circulation, lipids have to be hydrolyzed to small and simple molecules. Lipases, such as lipoprotein lipase (LPL) and endothelial lipase (EL), are key proteins expressed on the surface of trophoblast cells, where they hydrolyze esterified lipids from lipoproteins, so that they can be acquired by the placenta (Herrera et al 1987, Gauster et al 2007. Expression and activity of these transporters is a limiting step in lipid transport through the placenta to the fetus (Jones et al 2007, Duttaroy 2009).…”

Section: Introductionmentioning

confidence: 99%

Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

Mazzucco

Higa

Capobianco

et al. 2013

Journal of Endocrinology

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Metabolic alterations in obese and overweight mothers impact the placenta and the fetus, leading to anomalies in fetal growth and lipid accretion. The primary aim of the study was to examine the effect of a saturated fat-rich diet (FD) on growth, lipid accretion, and lipases, leptin and leptin receptor (ObR) expression in the placenta and fetal liver. We also aimed to find a role for fetal leptin in the modulation of placental and fetal liver lipase and ObR expression. Six-week-old rats were fed with a standard rat chow (control) or a 25% FD for 7 weeks until mating and during pregnancy. Also, in a group of control rats, fetuses were injected with leptin on days 19, 20, and 21 of pregnancy. On day 21, we assessed lipidemia, insulinemia, and leptinemia in mothers and fetuses. In the placenta and fetal liver, lipid concentration was assessed by thin layer chromatography (TLC) and the gene expression of lipoprotein lipase (LPL), endothelial lipase, insulin receptor (Insr), leptin, and ObR by RT-PCR. The FD induced hypertriglyceridemia and hyperleptinemia (P!0.01) in mothers and fetuses, an increase in maternal (P!0.05) and fetal weight (P!0.01), overaccumulation of lipids in fetal liver (P!0.01), and enhanced leptin expression in the placenta and fetal liver (P!0.05). Placental expression of IR and LPL was increased (P!0.05), and ObR decreased (P!0.05) in the FD group. Fetal administration of leptin induced the placental and fetal liver downregulation of ObR (P!0.05) and upregulation of LPL expression (P!0.05). The FD led to increased fetal lipid levels, which may result from high maternal lipid availability and fetal leptin effects. Key Words" Saturated fat-rich diet

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Section: Introductionmentioning

confidence: 99%

Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

Mazzucco

Higa

Capobianco

et al. 2013

Journal of Endocrinology

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“…Fat depots accumulate during the early stages of pregnancy and decrease during the late phases (7). Net catabolic changes taking place in adipose tissue during late pregnancy are manifested by an enhanced hormone-sensitive lipase (HSL) activity and decreased LPL activity (8), which result in an increase in maternal plasma lipids both in humans (9,10) and in rats (11,12).…”

mentioning

confidence: 99%

Expression, activity, and localization of hormone-sensitive lipase in rat mammary gland during pregnancy and lactation

Martín-Hidalgo¹,

Huerta²,

Álvarez³

et al. 2005

Journal of Lipid Research

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Mammary glands, besides being among the tissues in the body with the highest lipid content after adipose tissue (1), are one of the most active metabolic tissues in the body during pregnancy and lactation. Milk lipid is an important source of both calories and essential fatty acids for the newborn. During lactation, women secrete 800 ml of milk per day containing 4% fat, mostly corresponding to triacylglycerols, of which the mammary gland synthesizes ‫ف‬ 32 g daily (2). The lactating mouse mammary gland secretes 5 ml of milk per day containing ‫ف‬ 30% fat (3). To develop this transitory capacity for handling such a large amount of lipids, the morphology of the mammary tissue changes during pregnancy and lactation. In nonpregnant mammary glands, the predominant cells are adipocytes with epithelial structures interdispersed among them. During pregnancy, in mammary glands there is an extensive proliferation of alveolar structures into the adipocytes, accompanied by differentiation of epithelial cells (4), which show cytoplasmic lipid droplets (5) surrounded by the protein adipophilin (6). During lactation, epithelial cells are the predominant cell type, and only small channels of lipid-filled adipocytes and lipid-depleted adipocytes may be distinguished.During pregnancy, major changes in maternal lipid metabolism occur. Fat depots accumulate during the early stages of pregnancy and decrease during the late phases (7). Net catabolic changes taking place in adipose tissue during late pregnancy are manifested by an enhanced hormone-sensitive lipase (HSL) activity and decreased LPL activity (8), which result in an increase in maternal plasma lipids both in humans (9, 10) and in rats (11,12). The increments of triglyceride (TG)-rich lipoproteins (chylomicrons and VLDLs) are among the most pronounced changes in plasma lipids during late pregnancy (10,13,14). Reduced adipose tissue LPL activity during late gestation allows blood TG to be diverted from storage in adipose tissue to other tissues, such as mammary glands, where there is an induction in LPL expression and activity, allowing the subsequent hydrolysis and uptake of circulating TG in preparation for lactation (15,16).

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“…Tikkanen et al [17] administered estradiol valerate (2 mg/day for 3 months) to six postmenopausal women and produced suppression of HTGL but no suppression of LpL. Suppression of LpL could be seen only after high levels of estrogens, as during the third trimester of pregnancy [18], pancreatitis in pregnant women with hypertriglyceridemia [19], and hypertriglyceridemia with a high dose of estrogen to elderly women [20]. HTGL accelerates conversion of HDL2-C to HDL3-C and induces uptake of HDL by the liver [21].…”

Section: Discussionmentioning

confidence: 99%

Effect of Estrogen Replacement Therapy on Hepatic Triglyceride Lipase, Lipoprotein Lipase and Lipids Including Apolipoprotein E in Climacteric and Elderly Women.

et al. 1996

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Lipid Metabolism in Pregnancy

Cited by 84 publications

References 197 publications

Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

Saturated fat-rich diet increases fetal lipids and modulates LPL and leptin receptor expression in rat placentas

Expression, activity, and localization of hormone-sensitive lipase in rat mammary gland during pregnancy and lactation

Effect of Estrogen Replacement Therapy on Hepatic Triglyceride Lipase, Lipoprotein Lipase and Lipids Including Apolipoprotein E in Climacteric and Elderly Women.

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