Does high polyunsaturated free fatty acid level at the feto-maternal interface alter steroid hormone message during pregnancy?

Benassayag, C.; Rigourd, Virginie; Mignot, Thérèse-Marie; Hassid, J.; Leroy, Marie-Josèphe; Robert, Brigitte; Civel, C.; Grangé, G.; Dallot, Emmanuelle; Tanguy, Julie; Nunez, Emmanuel A.; Ferré, Françoise

doi:10.1016/s0952-3278(99)80019-2

Cited by 18 publications

(19 citation statements)

References 23 publications

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“…It suggests that progesterone is involved in the control of proliferation or differentiation and vasoactivity of the fetoplacental circulation, which are important events in placental vascular physiology and pathology, such as pre-eclampsia and intrauterine growth retardation. This may also occur on the maternal side, because progesterone receptors have been found in term decidual cells [39] and the myometria of pregnant women during late pregnancy [40].…”

Section: Discussionmentioning

confidence: 99%

Corticosteroid-Binding Globulin Status at the Fetomaternal Interface During Human Term Pregnancy1

Benassayag

Souski

Mignot

et al. 2001

Biology of Reproduction

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The status of the corticosteroid-binding globulin (CBG) at the fetomaternal interface, especially in the maternal intervillous blood space (I), was investigated and compared to that of CBG in the maternal (M) and fetal (umbilical arteries [A] and vein [V]) peripheral circulations at term. Immunoquantitation of plasma CBG showed that the CBG concentration in I was 30% less than that in M (P < 0.001) and threefold higher than that in umbilical cord blood (P < 0.001). The microheterogeneity of CBG studied by immunoaffinoelectrophoresis in the presence of concanavalin A and Western blotting indicated that the CBG in I was mainly of maternal origin and different from fetal CBG. A CBG mRNA, but no classic 50- to 59-kDa CBG, was found in isolated term trophoblastic cells. The steroid environment of the CBG in I differed greatly from that in the peripheral maternal and fetal circulations, because the progesterone:cortisol molar ratio in I was 75-fold higher than that in M and 7- to 10-fold higher than that in the fetal circulation. Binding studies revealed that the affinity constants of CBG for cortisol in I, A, and V were significantly lower than that in M plasma (P < 0.02) in their respective hormonal contexts. The binding parameters for I-CBG stripped of endogenous steroids and lipids were close to those for M-CBG but different from those of fetal CBG (P < 0.001). These data reflect the physiological relevance of the CBG-steroid interaction, especially with very CBG-loaded progesterone at the fetomaternal interface during late pregnancy.

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Section: Discussionmentioning

confidence: 99%

Corticosteroid-Binding Globulin Status at the Fetomaternal Interface During Human Term Pregnancy1

Benassayag

Souski

Mignot

et al. 2001

Biology of Reproduction

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“…The concentration of NEFA in the maternal plasma at term is around three times that in the fetal circulation, but the concentration of albumin, its primary carrier protein, is actually 10%-20% higher in the fetal than in the maternal circulation (4). This contrasts with the other lipoprotein fractions that carry the esterified lipids, as these actually decrease in the fetal circulation with increasing gestation (5,109). As a result of these changes, the ratio of plasma NEFA to albumin on the fetal side of the placenta is around a quarter of that on the maternal side at term (5).…”

Section: The Driver Of Placental Fatty Acid Transportmentioning

confidence: 97%

“…This contrasts with the other lipoprotein fractions that carry the esterified lipids, as these actually decrease in the fetal circulation with increasing gestation (5,109). As a result of these changes, the ratio of plasma NEFA to albumin on the fetal side of the placenta is around a quarter of that on the maternal side at term (5). NEFAs in the fetal circulation are also carried on α-fetoprotein, which has a similar molar fatty acid-loading capacity to albumin (2-3 moles per mole protein), but this protein is only present in the fetal plasma at concentrations around one thousand times lower than albumin (5); therefore, its contribution to overall binding capacity in the fetal circulation is negligible.…”

Section: The Driver Of Placental Fatty Acid Transportmentioning

confidence: 97%

Fatty Acid Supply to the Human Fetus

2010

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Deposition of fat in the fetus increases exponentially with gestational age, reaching its maximal rate-around 7 g/day or 90% of energy deposition-at term. In late pregnancy, many women consuming contemporary Western diets may not be able to meet the fetal demand for n-3 long chain polyunsaturated fatty acids (LCPUFAs) from the diet alone. Numerous mechanisms have evolved to protect human offspring from extreme variation or deficiency in the maternal diet during pregnancy. Maternal adipose tissue is an important source of LCPUFA. Temporal changes in placental function are synchronized with maternal metabolic and physiological changes to ensure a continuous supply of n-3 and n-6 LCPUFA-enriched fat to the fetus. LCPUFA storage in fetal adipose tissue provides an important source of LCPUFA during the critical first months of postnatal life. An appreciation of these adaptations is important in any nutritional strategy designed to improve the availability of fatty acids to the fetus.

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“…Figure 2 Fatty acids may be found in the blood and tissues linked to other molecules by ester bonds; triglyceride (TG), phospholipid (PL) and cholesterol ester (CE); or as non-esterified fatty acids NEFA. AA and DHA as a proportion of total fatty acids are shown for the diet of pregnant mothers (Lakin et al, 1998), 1 the adipose tissue (Leaf et al, 1995), 2 maternal and cord blood plasma phospholipids (Otto et al, 1997), 3 triglyceride (Berghaus et al, 2000), 4 cholesterol ester (Hoving et al, 1994), 5 and NEFA (Benassayag et al, 1999), 6 the placental microvillous and basal membranes (Powell et al, 1999), 7 and adipose tissue and brain at birth (Clandinin et al, 1981 Figure 3 The theoretical rate of oxidation was calculated from the rate of maternal energy expenditure (9453 MJ/day), the proportion of that energy derived from fat (30%), the energy content of fat (39 kJ/g) (Butte, 2000) and the proportion of DHA in the oxidised fat (0.1% DHA; Figure 2). The DHA content of fetal tissues was calculated from the lean mass (calculated as body weight minus the weight of fat, skeleton and skin (Widdowson, 1974)), the fat mass (Widdowson, 1974) and the weight of the placenta (Hytten, 1974) and brain (Clandinin et al, 1980) and the fat and DHA concentration of the brain (Clandinin et al, 1980;Jamieson et al, 1999), placenta (Widdowson & Spray, 1951;Lakin et al, 1998) and adipose tissue (Clandinin et al, 1981).…”

Section: Importance Of Fatty Acids To the Fetusmentioning

confidence: 99%

“…The NEFA concentration difference between the maternal and fetal circulation increases throughout gestation until term when the concentration of NEFA in the maternal plasma at term is approximately three times that in the fetal circulation. However, the concentration of its primary carrier protein, albumin, is actually 10-20% higher in the fetal than maternal circulation (Benassayag et al, 1997(Benassayag et al, , 1999. Consequently, the ratio of plasma NEFA to albumin on the fetal side of the placenta is around a third of that on the maternal side (Benassayag et al, 1999), and it is this gradient that drives the maternal to fetal transfer of fatty acids.…”

Section: Maternalmentioning

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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Does high polyunsaturated free fatty acid level at the feto-maternal interface alter steroid hormone message during pregnancy?

Cited by 18 publications

References 23 publications

Corticosteroid-Binding Globulin Status at the Fetomaternal Interface During Human Term Pregnancy1

Corticosteroid-Binding Globulin Status at the Fetomaternal Interface During Human Term Pregnancy1

Fatty Acid Supply to the Human Fetus

Effect of placental function on fatty acid requirements during pregnancy

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