Essential fatty acid deficiency and brain development

Menon, N. K.; Dhopeshwarkar, Govind A.

doi:10.1016/0163-7827(82)90013-3

Cited by 74 publications

(23 citation statements)

References 77 publications

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“…Essential fatty acids R Uauy et al S67 from humans have established that brain phospholipid DHA decreases while n-9 and n-7 mono-and polyunsaturated fatty acids increase when LA and LNA or only n-3 fatty acids are de®cient in the diet (Galli et al, 1971;Menon & Dhopeshwarkar, 1982;Bourre et al, 1989a). Typically, n-3 fatty acid de®cient cells have decreased DHA and increased levels of the end products of n-6 metabolism, docosapentaenoic acid (DPA).…”

Section: Basis For Nutritional Essentiality Of Efas and Derivativesmentioning

confidence: 99%

“…Typically, n-3 fatty acid de®cient cells have decreased DHA and increased levels of the end products of n-6 metabolism, docosapentaenoic acid (DPA). Within the subcellular organelles, synaptosomes and mitochondria seem to be more sensitive to a low dietary n-3 supply (Menon & Dhopeshwarkar, 1982;Bourre et al, 1989b).…”

Section: Basis For Nutritional Essentiality Of Efas and Derivativesmentioning

confidence: 99%

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Essential fatty acids as determinants of lipid requirements in infants, children and adults

1999

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Section: Basis For Nutritional Essentiality Of Efas and Derivativesmentioning

confidence: 99%

Section: Basis For Nutritional Essentiality Of Efas and Derivativesmentioning

confidence: 99%

Essential fatty acids as determinants of lipid requirements in infants, children and adults

1999

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“…is present in mammalian brain lipid at many times the concentration of 20:5(n-3), but is also chain elongated and desaturated (Sinclair 1976;Crawford et al 1976). Therefore 22:4(n-6) is normally a significant component of the total fatty acids (Sinclair 1975;Crawford et al 1976), but 22:5(n-6) is present in smaller amounts and only becomes a significant component in (n-3)PUFA deficiency when brain 22:6(n-3) levels are reduced (Menon and Dhopeshwarkar 1982;Neuringer et al 1986). However, 20:4(n-6) is only a minor PUFA in fish tissue lipids and its longer chain metabolities are very rarely reported in fish lipid fatty acid compositions (Ackman 1980(Ackman , 1982Henderson and Tocher 1987).…”

Section: Introductionmentioning

confidence: 99%

Fatty acid compositions of the major phosphoglycerides from fish neural tissues; (n−3) and (n−6) polyunsaturated fatty acids in rainbow trout (Salmo gairdneri) and cod (Gadus morhua) brains and retinas

Tocher

Harvie

1988

Fish Physiol Biochem

333

225

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The fatty acid compositions of brain phosphoglycerides from a freshwater fish, the rainbow trout (Salmo gairdneri), and a marine fish, the cod (Gadus morhua), were determined and compared with those from a terrestrial mammal, the rat. Fish brain lipids were characterized by a higher degree of unsaturation encompassing increased percentages of (n-3)PUFA (22∶6 and 20∶5) and lower percentages of (n-6)PUFA (20∶4 and 22∶4). However the distribution of fatty acids and specific PUFA between different phosphoglycerides was essentially similar in rat and fish brain tissue. PE and PS contained the highest percentages of 22∶6(n-3), PI was characterized by higher 18∶0 and 20∶4(n-6)/20∶5(n-3), and PC had higher 16∶0 and the lowest percentage of PUFA in all species. A generally similar pattern was found in the fish retinal phosphoglycerides except that PC was also rich in 22∶6(n-3). Overall trout brain phosphoglycerides were slightly more unsaturated than the cod lipids but with lower (n-3)/(n-6) ratios whereas cod retinal lipids were more unsaturated than the trout retinal lipids.

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“…Some studies have demonstrated that intrauterine growth retardation could be due to a deficiency in essential fatty acids intake by the mother during pregnancy, especially in linoleic and a-linoleic acids (~is-~is-d~~'~-octadecadienoic acid) [13,141. Recent studies in humans and animals, demonstrated that a mild deficiency in essential fatty acid intake could limit fetal growth processes, while the maternal dietary supplementation could prevent intrauterine growth retardation [14].…”

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confidence: 99%

Linoleic Acid Transport by Human Placental Syncytiotrophoblast Membranes

Lafond¹,

Simoneau²,

Savard³

et al. 1994

European Journal of Biochemistry

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The placenta syncytiotrophoblast is the site of exchange of nutrients, lipids and minerals between the mother and the fetus. In order to characterize the transport of fatty acids by the placenta, we purified bipolar syncytiotrophoblast brush border and basal plasma membranes from human placenta. These purified brush border and basal plasma membranes enriched 3-fold and 22-fold, respectively, in sodiudpotassium-ATPase and 27-fold and 6-fold in alkaline phosphatase activity, compared with the placental homogenates. Fatty acid transport was performed at different fatty acid albumin ratios to evaluate the optimal uptake conditions. The maximal transport efficiency, for linoleic acid bound to albumin by sonication, was obtained with a 6 : 1 fatty acidalbumin ratio in brush border and basal plasma membranes. The linoleic acid transport observed with brush border membranes followed Michaelis-Menten kinetics, with a Michaelis constant of 7.89 ? 0.01 pM and a maximal incorporation rate of 30.80 ? 6.39 pmol . mg-' . min-I. Linoleic acid transport was very low in basal plasma membranes and we obtained a Michaelis constant of 0.95 2 0.01 yM and a maximal incorporation rate of 1.62 +-5.06 pmol . mg-' . mine '. In order to show that linoleic acid accumulated within brush border and plasma membrane vesicles, and to eliminate the possibility of a non-specific binding of fatty acid to these membranes, we demonstrated by an osmolarity experiment, the decrease of the linoleic acid transport in brush border and basal plasma membranes obtained in the presence of 455 pM essential fatty acid at 23°C for 180 min. The results presented in this study suggest that linoleic acid is transported significantly by syncytiotrophoblast brush border membranes and basal plasma membranes. Thus, it may represent a unidirectional transport from mother to fetus through the brush border membranes facing the mother, followed by transport at a slower rate through basal plasma membranes facing the fetus.Fatty acids are required for adequate fetal development and growth. These fatty acids can be synthesized by the placenta [I, 21 or can be provided by external sources including the maternal circulation. The amount of fatty acids transported by the placenta to the fetus varies between species [3]. In the ruminant and feline fetus, with epitheliochorial and hemoendothelial placentation, respectively, the amount of fatty acids transported by the placenta is less important than in species with hemochorial placentation (e.g. humans) [4-61. In a review article, Coleman has reported that fatty acid transport seems to be affected by maternal nutrition and stages of gestation [7]. Essential fatty acids are provided only by the maternal diet because the metabolic enzymes required for their synthesis are not present in fetuses of mammals [7, 81. In the last trimester of pregnancy, these essential fatty acids are very important for the growth and the development of the nervous system [9, lo], for the elaboration of cellular Correspondence to J. Lafond, Universite du...

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Essential fatty acid deficiency and brain development

Cited by 74 publications

References 77 publications

Essential fatty acids as determinants of lipid requirements in infants, children and adults

Essential fatty acids as determinants of lipid requirements in infants, children and adults

Fatty acid compositions of the major phosphoglycerides from fish neural tissues; (n−3) and (n−6) polyunsaturated fatty acids in rainbow trout (Salmo gairdneri) and cod (Gadus morhua) brains and retinas

Linoleic Acid Transport by Human Placental Syncytiotrophoblast Membranes

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