Marine lipids
Chez les animaux ayant reçu le 18:3 (n-3), 59 % de cet acide gras polyinsaturé ont disparu β-oxydation apparente), 0,5 % ont été excrétés,
21 % accumulés tels quels (50 % dans les tissus adipeux et 46 % dans
le compartiment carcasse-peau) et 19 % convertis en homologues supérieurs (dont 14 % en DHA).
Les résultats obtenus après ingestion du DHA sont comparables (disparition : 62,5 % ; excretion : 0,5 % ; accumulation : 37 % dont 30 % de
DHA et 7 % de 20:5 (n-3) + 22:5 (n-3). Contrairement au 18:3 (n-3),
le DHA est essentiellement incorporé dans le compartiment carcassepeau (68 % ).
En conclusion, le statut suboptimal en DHA des enfants allaités artificiellement ne résulterait pas d’un taux spécifiquement élevé de β-oxydation du 18:3 (n-3).
Introduction
Docosahexaenoic acid (DHA, 22: (6n-3) is present at high concentrations
in the structural lipids of excitable membranes in brain and retina
(Innis, 1991). In the human species, it is mainly synthesized through
endogenous alternative desaturation-elongation pathway from the
essential fatty acid α-linolemc acid ( 18:3 (n-3), which is the major form
of fat dietary supply. The DHA deposition primarily occurs during brain
development. An a-linolenic acid dietary deficiency in rodents and
non-human primates during this period induces a depletion of DHA in
nervous tissues and provokes an impairment of visual and cognitive development (Innis, 1991 ; Connor et al., 1992). Similar visual alteration was
also observed in newborn infants fed low a-linolenic acid formulas
(Uauy et al., 1990; Birch et al., 1992). These experimental studies show
that n-3 fatty acids are essential to normal neurophysiological development and suggest a minimal requirement for a-linolenic acid in
newborn infants of 0.5% kcal (i.e. 1.0 weight % of total fatty acids in
formulas) (ESPGAN, 1991). Whatever the α-linolenic acid dietary
supply, the DHA content of plasma, erythrocytes and cerebral cortex phospholipids in formula-fed infants is lower than that of breast-fed infants
(Maurage et al., 1998). This difference, which is due to the specific
presence of DHA in human milk (up to 0.2-0.5 weight % for women
living in western countries), dissappears when formulas are supplemented with DHA (Maurage et al., 1998).
Dose-response studies in animals have also shown that DHA content in
brain and retina plateauecl at a higher value when (n-3) fatty acids are
provided as DHA. This difference in DHA accretion in nervous tissues
during perinatal development could be due mainly to a higher β-oxidation rate of α-linolenic acid and/or an immature activity of the
desaturation-elongation pathway.
The aim of our study was to determine the β-oxidation rate of DHA
because to our knowledge, there is no data on this subject in the literature. In tlns purpose, we determined β-oxidation (i.e. disappearance)
156
Chez les animaux ayant reçu le 18:3 (n-3), 59 % de cet acide gras polyinsaturé ont disparu β-oxydation apparente), 0,5 % ont été excrétés,
21 % accumulés tels quels (50 % dans les tissus adipeux et 46 % dans
le compartiment carcasse-peau) et 19 % convertis en homologues supérieurs (dont 14 % en DHA).
Les résultats obtenus après ingestion du DHA sont comparables (disparition : 62,5 % ; excretion : 0,5 % ; accumulation : 37 % dont 30 % de
DHA et 7 % de 20:5 (n-3) + 22:5 (n-3). Contrairement au 18:3 (n-3),
le DHA est essentiellement incorporé dans le compartiment carcassepeau (68 % ).
En conclusion, le statut suboptimal en DHA des enfants allaités artificiellement ne résulterait pas d’un taux spécifiquement élevé de β-oxydation du 18:3 (n-3).
Introduction
Docosahexaenoic acid (DHA, 22: (6n-3) is present at high concentrations
in the structural lipids of excitable membranes in brain and retina
(Innis, 1991). In the human species, it is mainly synthesized through
endogenous alternative desaturation-elongation pathway from the
essential fatty acid α-linolemc acid ( 18:3 (n-3), which is the major form
of fat dietary supply. The DHA deposition primarily occurs during brain
development. An a-linolenic acid dietary deficiency in rodents and
non-human primates during this period induces a depletion of DHA in
nervous tissues and provokes an impairment of visual and cognitive development (Innis, 1991 ; Connor et al., 1992). Similar visual alteration was
also observed in newborn infants fed low a-linolenic acid formulas
(Uauy et al., 1990; Birch et al., 1992). These experimental studies show
that n-3 fatty acids are essential to normal neurophysiological development and suggest a minimal requirement for a-linolenic acid in
newborn infants of 0.5% kcal (i.e. 1.0 weight % of total fatty acids in
formulas) (ESPGAN, 1991). Whatever the α-linolenic acid dietary
supply, the DHA content of plasma, erythrocytes and cerebral cortex phospholipids in formula-fed infants is lower than that of breast-fed infants
(Maurage et al., 1998). This difference, which is due to the specific
presence of DHA in human milk (up to 0.2-0.5 weight % for women
living in western countries), dissappears when formulas are supplemented with DHA (Maurage et al., 1998).
Dose-response studies in animals have also shown that DHA content in
brain and retina plateauecl at a higher value when (n-3) fatty acids are
provided as DHA. This difference in DHA accretion in nervous tissues
during perinatal development could be due mainly to a higher β-oxidation rate of α-linolenic acid and/or an immature activity of the
desaturation-elongation pathway.
The aim of our study was to determine the β-oxidation rate of DHA
because to our knowledge, there is no data on this subject in the literature. In tlns purpose, we determined β-oxidation (i.e. disappearance)
156