[Essential fatty acids and prematurity: a triple experimental approach].

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Descomps B, Rodriguez A

[Essential fatty acids and prematurity: a triple experimental approach].

C R Seances Soc Biol Fil. 1995;189(5):781-96.

PubMed ID

8673626 [ View in PubMed

]

Abstract

Previous studies in our laboratory have shown that in fetal plasma arachidonic (AA) and docosahexaenoic acid (DHA) levels are higher (about two fold) than in maternal plasma whereas the reverse situation was observed for the levels of their C18 precursors linoleic acid (AL) and alpha-linolenic acid (AAL) (13). This paradoxical situation raises the questions of the origin of the long chain polyunsaturated fatty acids (PUFAs) and of the ability of fetal liver to desaturate and elongate C18 precursors since placenta was shown not to be able to desaturate fatty acids. This question should be answered for the rationale of formula feeding supplementation either with long chain PUFAs or with their C18 precursors. Three experimental approaches can contribute to elucidate this dilemna: nutritional studies with formula supplementation, investigations on hepatic enzymes in vitro, in vivo experiments using stable isotopes. Supplementation of formulas with AAL in precise conditions (AL/AAL ratio: 6.4/1 and AL intake: 4.95% of total energetic supply) was done in a multicentric study including 88 premature newborns (32 weeks post conceptional age) for five weeks. The plasma phospholipid and red blood cell DHA status was found to be closer to human milk feeding than with standard formula feeding and most of the n-6 pathway was preserved. The data suggests that in premature newborns a significant conversion of AAL into DHA is possible provided an equilibrium is respected between AL and AAL supplies. This conversion is confirmed both by in vitro and in vivo studies: in fetal livers (obtained from therapeutic abortion) significant delta 6 and delta 5 desaturase activities were measured by a radiochemical method using reverse phase HPLC separation of [1-14C] labelled substrates and products in the n-6 and in the n-3 series. Substrate inhibition was observed especially at delta 5 desaturation and the maximum velocities were relatively limited mainly in the n-6 pathway which was slower than in the n-3 serie. These data are in agreement with recent preliminary data obtained in different laboratories with stable isotopes in vivo but in infants born in term: experiments using either 13C or deuterium labelled fatty acids concluded to the conversion of C18 essential fatty acids into AA and DHA justifying (AAL) formula supplementation for sustaining DHA status in preterm newborns.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
alpha-Linolenic acid	Fatty acid desaturase 1	Protein	Humans	Yes	Ligand	Details