Pathway of α-linolenic acid through the mitochondrial outer membrane in the rat liver and influence on the rate of oxidation. Comparison with linoleic and oleic acids

The movement of alpha-linolenic acid (C18:3, n-3) through the mitochondrial outer membrane to oxidation sites was studied in rat liver and compared with the movement of linoleic acid (C18:2, n-6) and oleic acid (C18:1, n-9). All differ in the degree of unsaturation, but have the same chain length and the same position of the first double bond when counted from the carboxyl end. The following results were obtained. (1) The overall beta-oxidation in total mitochondria was in the order C18:3, n-3 greater than C18:2, n-6 greater than C18:1, n-9, independent of the amount of albumin in the medium. (2) The rate of formation of acylcarnitine from acyl-CoA was higher with oleoyl-CoA than with linoleoyl-CoA, and remained very low with alpha-linolenoyl-CoA for all concentrations studied. (3) When the formation of acylcarnitines originated from fatty acids (as potassium salts) in a medium containing CoA and ATP, the conversion of alpha-linolenate was greater than that of linoleate, which in turn was greater than that of oleate. (4) Use of a more purified mitochondrial fraction, practically devoid of peroxisomes, did not modify the results obtained with alpha-linolenate. (5) alpha-Linolenoyl-CoA did not inhibit oxidation of labelled alpha-linolenate, whereas the other acyl-CoAs did. (6) Transfer to carnitine of all three fatty acids (as potassium salts) by carnitine palmitoyltransferase-I (CPT-I) was similarly inhibited by increasing concentrations of malonyl-CoA. (7) On using a fraction containing mitochondrial outer membranes, the formation of acylcarnitines from potassium salts of fatty acids was qualitatively and quantitatively similar to that found with whole mitochondria. (8) Our observations show that alpha-linolenoyl-CoA synthesized other than in the mitochondria cannot be used to any great extent by the mitochondria due to its configuration. However when added as the unactivated form, alpha-linolenate appears to be very quickly oxidized, but should first be activated by acyl-CoA synthetase in the mitochondrion itself. Then it is rapidly channelled to CPT-I. These enzymic sites are probably close together in the mitochondrial outer membrane. The different behaviour of the alpha-linolenic group compared with the other acyl groups in the studied pathway can be explained by a different spatial arrangement due to the number and position of the double bonds.</jats:p

Particularité du passage de l'acide α-linolénique à travers la membrane mitochondriale externe : comparaison avec les acides palmitique et oléique

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β-lactoglobulin as a molecular carrier of linoleate: characterisation and effects on intestinal epithelial cells in vitro

S. Le Maux is currently supported by a Teagasc Walsh Fellowship and the Department of Agriculture, Fisheries and Food (FIRM project 08/RD/TMFRC/650). We also acknowledge funding from IRCSET-Ulysses Travel Grant.peer-reviewedThe dairy protein β-lactoglobulin (βlg) is known to bind hydrophobic ligands such as fatty acids. In the present work, we investigated the biological activity in vitro of linoleate once complexed to bovine βlg. Binding of linoleate (C18:2) to bovine βlg was achieved by heating at 60 °C for 30 min at pH 7.4, resulting in a linoleate/βlg molar binding stoichiometry of 1.1, 2.1, and 3.4. Two types of binding sites were determined by ITC titrations. Binding of linoleate induced the formation of covalent dimers and trimers of βlg. The LD50 on Caco-2 cells after 24 h was 58 μM linoleate. However, cell viability was unaffected when 200 μM linoleate was presented to the Caco-2 cells as part of the βlg complex. The Caco-2 cells did not increase mRNA transcript levels of long chain fatty acid transport genes, FATP4 and FABPpm, or increase levels of the cAMP signal, in response to the presence of 50 μM linoleate alone or as part of the βlg complex. Therefore, it is proposed that βlg can act as a molecular carrier and alter the bioaccessibility of linoleate/linoleic acid

Les CLA, “nouveaux nutriments fonctionnels” ?

Les diènes conjugués de l’acide linoléique (CLA) constituent un groupe d’acides gras atypiques produits au cours de l’hydrogénation progressive de l’acide linoléique. Dans différentes espèces de mammifère, les mélanges isomériques commerciaux vendus comme compléments alimentaires provoquent d’une chute plus ou moins marquée de la masse grasse. Cet effet anti-obésité est strictement dépendant de l’isomère t10,c12-CLA trouvé normalement à l’état de trace dans l’alimentation. Chez la souris, la consommation chronique de cet isomère entraîne l’apparition d’un syndrome complexe caractérisé par une lipoatrophie, une hyperinsulinémie, une insulinorésistance et une stéatose hépatique dont l’origine et la chronologie sont présentées et commentées dans cette synthèse. Chez l’Homme, l’impact des CLA sur la masse grasse est anecdotique. Cependant, des essais cliniques indiquent que la consommation de t10,c12-CLA peut s’accompagner d’effets secondaires indésirables. L’introduction de mélanges de CLA riches en t10,c12-CLA dans l’alimentation humaine ne semble donc pas justifiée, que ce soit sous forme de compléments ou sous forme d’ingrédients alimentaires