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      Maternal Lipid Metabolism and Placental Lipid Transfer

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          During early pregnancy, long-chain polyunsaturated fatty acids (LC-PUFA) may accumulate in maternal fat depots and become available for placental transfer during late pregnancy, when the fetal growth rate is maximal and fetal requirements for LC-PUFAs are greatly enhanced. During this late part of gestation, enhanced lipolytic activity in adipose tissue contributes to the development of maternal hyperlipidaemia; there is an increase in plasma triacylglycerol concentrations, with smaller rises in phospholipid and cholesterol concentrations. Besides the increase in plasma very-low-density lipoprotein, there is a proportional enrichment of triacylglycerols in both low-density lipoproteins and high-density lipoproteins. These lipoproteins transport LC-PUFA in the maternal circulation. The presence of lipoprotein receptors in the placenta allows their placental uptake, where they are hydrolysed by lipoprotein lipase, phospholipase A<sub>2</sub> and intracellular lipase. The fatty acids that are released can be metabolized and diffuse into the fetal plasma. Although present in smaller proportions, maternal plasma non-esterified fatty acids are also a source of LC-PUFA for the fetus, their placental transfer being facilitated by the presence of a membrane fatty acid-binding protein. There is very little placental transfer of glycerol, whereas the transfer of ketone bodies may become quantitatively important under conditions of maternal hyperketonaemia, such as during fasting, a high-fat diet or diabetes. The demands for cholesterol in the fetus are high, but whereas maternal cholesterol substantially contributes to fetal cholesterol during early pregnancy, fetal cholesterol biosynthesis rather than cholesterol transfer from maternal lipoproteins seems to be the main mechanism for satisfying fetal requirements during late pregnancy.

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          Most cited references 17

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          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.

          To determine whether oxidized LDL enhances atherogenesis by promoting monocyte recruitment into the vascular intima, we investigated whether LDL accumulation and oxidation precede intimal accumulation of monocytes in human fetal aortas (from spontaneous abortions and premature newborns who died within 12 h; fetal age 6.2+/-1.3 mo). For this purpose, a systematic assessment of fatty streak formation was carried out in fetal aortas from normocholesterolemic mothers (n = 22), hypercholesterolemic mothers (n = 33), and mothers who were hypercholesterolemic only during pregnancy (n = 27). Fetal plasma cholesterol levels showed a strong inverse correlation with fetal age (R = -0.88, P < 0.0001). In fetuses younger than 6 mo, fetal plasma cholesterol levels correlated with maternal ones (R = 0.86, P = 0.001), whereas in older fetuses no such correlation existed. Fetal aortas from hypercholesterolemic mothers and mothers with temporary hypercholesterolemia contained significantly more and larger lesions (758,651+/-87,449 and 451,255+/-37,448 micron2 per section, respectively; mean+/-SD) than aortas from normocholesterolemic mothers (61,862+/-9,555 micron2; P < 0.00005). Serial sections of the arch, thoracic, and abdominal aortas were immunostained for recognized markers of atherosclerosis: macrophages, apo B, and two different oxidation-specific epitopes (malondialdehyde- and 4-hydroxynonenal-lysine). Of the atherogenic sites that showed positive immunostaining for at least one of these markers, 58.6% were established lesions containing both macrophage/foam cells and oxidized LDL (OxLDL). 17.3% of all sites contained only native LDL, and 13.3% contained only OxLDL without monocyte/ macrophages. In contrast, only 4.3% of sites contained isolated monocytes in the absence of native or oxidized LDL. In addition, 6.3% of sites contained LDL and macrophages but few oxidation-specific epitopes. These results demonstrate that LDL oxidation and formation of fatty streaks occurs already during fetal development, and that both phenomena are greatly enhanced by maternal hypercholesterolemia. The fact that in very early lesions LDL and OxLDL are frequently found in the absence of monocyte/macrophages, whereas the opposite is rare, suggests that intimal LDL accumulation and oxidation contributes to monocyte recruitment in vivo.
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            Oxidative stress in term small for gestational age neonates born to undernourished mothers: a case control study

            Background The objective of this study was to assess the status of oxidative stress in term small for gestational age (SGA) newborn infants born to undernourished mothers by estimating levels of erythrocyte superoxide dismutase (SOD), catalase, reduced glutathione, and serum malondialdehyde (MDA) in cord blood and comparing them to healthy appropriate for gestational age (AGA) controls. This was done in a case control design at a tertiary level teaching hospital. Methods We included 20 singleton healthy SGA newborn infants born between 38–40 weeks to undernourished mothers with a) post-pregnancy weight < 50 kg or height < 145 cm AND b) hemoglobin < 8.0 g/dL or serum albumin < 2.5 g/dL. An equal number of age and sex matched AGA newborn infants born to healthy mothers served as Controls. Mothers with other risk factors and newborns with complications during delivery or immediate newborn period were excluded. MDA, SOD, catalase and reduced glutathione were measured in the cord blood of all neonates and compared between the groups (unpaired t test); levels were also correlated to maternal weight, height, hemoglobin, and albumin by both univariate (pearsonian correlation) and multivariate (multiple regression) analysis. Results The activity of MDA was increased (5.33 ± 0.72 vs 2.55 ± 0.22 nmol/mL; P < 0.0001) while levels of superoxide dismutase (493.6 ± 54.9 vs. 786.8 ± 79.1 U/g Hb; P < 0.0001), catalase (1.48 ± 0.24 vs. 2.31 ± 0.20 U/g Hb; P < 0.0001) and reduced glutathione (2.84 ± 0.37 vs 6.42 ± 0.23 Umol/g Hb, P < 0.0001) were decreased in term SGA born to undernourished mothers as compared to term AGA born to healthy mothers. On univariate analysis, all the markers of oxidative stress correlated significantly with maternal parameters (P < 0.005). On multivariate analysis, maternal albumin and hemoglobin accounted for maximum correlation with the markers of oxidative stress. Conclusions Intrauterine malnutrition is associated with significant oxidative stress in small for gestational age neonates born at term to malnourished mothers.
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              The timing factor in the pathophysiology of the intrauterine growth retardation syndrome.

              Three different types of intrauterine growth retardation can be identified depending on the moment at which supplies to the fetus are diminished. When a reduction in sustenance occurs early in the first trimester of pregnancy, a well-proportioned but growth-retarded baby may be expected. When the negative factors develop around the 30th week of pregnancy, the result is a disproportionately growth-retarded infant. Both types of retardation can be illustrated using longitudinal uterine height and biparietal diameter values and by neonatal anthropometry. Epidemiological examples exist defining factors which produce these two kinds of retardation. The third type occurs when a reduction in food supplies takes place in the last month of pregnancy and causes a depletion of the fetal fat stored. Weight retardation is observed with little or no height impairment. In planning public health activities such as nutrition interventions for developing countries, the type of intrauterine growth retardation present in the target population should be considered in order to determine which type of intervention would be most appropriate, and establish its correct timing.

                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                April 2006
                10 April 2006
                : 65
                : Suppl 3
                : 59-64
                Department of Biochemistry, Molecular and Cellular Biology, University San Pablo-CEU, Madrid, Spain
                91507 Horm Res 2006;65:59–64
                © 2006 S. Karger AG, Basel

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                Page count
                Figures: 3, References: 33, Pages: 6
                The Biology of Fetal Growth


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