Florent Joffre

Multiscale structures of lipids in foods as parameters affecting fatty acid bioavailability and lipid metabolism.

On a nutritional standpoint, lipids are now being studied beyond their energy content and fatty acid (FA) profiles. Dietary FA are building blocks of a huge diversity of more complex molecules such as triacylglycerols (TAG) and phospholipids (PL), themselves organised in supramolecular structures presenting different thermal behaviours. They are generally embedded in complex food matrixes. Recent reports have revealed that molecular and supramolecular structures of lipids and their liquid or solid state at the body temperature influence both the digestibility and metabolism of dietary FA. The aim of the present review is to highlight recent knowledge on the impact on FA digestion, absorption and metabolism of: (i) the intramolecular structure of TAG; (ii) the nature of the lipid molecules carrying FA; (iii) the supramolecular organization and physical state of lipids in native and formulated food products and (iv) the food matrix. Further work should be accomplished now to obtain a more reliable body of evidence and integrate these data in future dietary recommendations. Additionally, innovative lipid formulations in which the health beneficial effects of either native or recomposed structures of lipids will be taken into account can be foreseen.

Differential effect of maternal diet supplementation with α-Linolenic acid or n-3 long-chain polyunsaturated fatty acids on glial cell phosphatidylethanolamine and phosphatidylserine fatty acid profile in neonate rat brains

BackgroundDietary long-chain polyunsaturated fatty acids (LC-PUFA) are of crucial importance for the development of neural tissues. The aim of this study was to evaluate the impact of a dietary supplementation in n-3 fatty acids in female rats during gestation and lactation on fatty acid pattern in brain glial cells phosphatidylethanolamine (PE) and phosphatidylserine (PS) in the neonates.MethodsSprague-Dawley rats were fed during the whole gestation and lactation period with a diet containing either docosahexaenoic acid (DHA, 0.55%) and eicosapentaenoic acid (EPA, 0.75% of total fatty acids) or α-linolenic acid (ALA, 2.90%). At two weeks of age, gastric content and brain glial cell PE and PS of rat neonates were analyzed for their fatty acid and dimethylacetal (DMA) profile. Data were analyzed by bivariate and multivariate statistics.ResultsIn the neonates from the group fed with n-3 LC-PUFA, the DHA level in gastric content (+65%, P < 0.0001) and brain glial cell PE (+18%, P = 0.0001) and PS (+15%, P = 0.0009) were significantly increased compared to the ALA group. The filtered correlation analysis (P < 0.05) underlined that levels of dihomo-γ-linolenic acid (DGLA), DHA and n-3 docosapentaenoic acid (DPA) were negatively correlated with arachidonic acid (ARA) and n-6 DPA in PE of brain glial cells. No significant correlation between n-3 and n-6 LC-PUFA were found in the PS dataset. DMA level in PE was negatively correlated with n-6 DPA. DMA were found to occur in brain glial cell PS fraction; in this class DMA level was correlated negatively with DHA and positively with ARA.ConclusionThe present study confirms that early supplementation of maternal diet with n-3 fatty acids supplied as LC-PUFA is more efficient in increasing n-3 in brain glial cell PE and PS in the neonate than ALA. Negative correlation between n-6 DPA, a conventional marker of DHA deficiency, and DMA in PE suggests n-6 DPA that potentially be considered as a marker of tissue ethanolamine plasmalogen status. The combination of multivariate and bivariate statistics allowed to underline that the accretion pattern of n-3 LC-PUFA in PE and PS differ.

Kinetic parameters of hepatic oxidation of cyclic fatty acid monomers formed from linoleic and linolenic acids.

Cyclic fatty acid monomers (CFAM) occur from linoleic (CFAM-18:2) or linolenic (CFAM-18:3) acids present in some edible oils as a result of domestic frying or industrial refining. They present adverse effects in pups and weaning rats. In the present work, we studied the importance of hepatic oxidation in the metabolism of CFAM. For this purpose, kinetic parameters of Carnitine Palmitoyl Transferase I (key enzyme of the channeling of the fatty acids into the mitochondrial beta-oxidation pathway) and Acyl CoA Oxidase (key enzyme of the peroxisomal oxidation pathway) towards CFAM-18:2 and CFAM-18:3 were calculated on hepatic sub-cellular fractions of rats. For mitochondrial oxidation of CFAM, we observed a lower oxygen consumption and a lower activity of Carnitine Palmitoyl Transferase compared to 18:2w6 and 16:0. For peroxisomal oxidation, CFAM-18:2 showed the same kinetic parameters (Vm and K(0.5)) as 18:2w6 and 16:0, used for oxidative controls, whereas CFAM-18:3 presented a lower Vm (-50%). This difference should induce a lower catabolism of CFAM-18:3 in liver. This could contribute to their accumulation and probably to their toxic effect.

Peroxisome proliferator-activated receptor α is not the exclusive mediator of the effects of dietary cyclic FA in mice

Cyclic FA monomers (CFAM) formed during heating of α-linolenic acid have been reported to interfere in hepatic metabolism in a putatively peroxisome proliferator-activated receptor α (PPARα)-dependent manner. In the present work, CFAM (0.5% of the diet) were administered for 3 wk to wild-type and PPARα-null mice of both genders to elucidate the role of PPARα in mediating the effects of CFAM on the activity of acyl-CoA oxidase (ACO) and ω-laurate hydroxylase (CYP4A), the regulation of which is known to be dependent on the PPARα. Dietary CFAM enhanced CYP4A activity threefold in male and female wild-type mice. This effect was abolished in PPARα-null mice. A twofold induction of ACO activity was found in wild-type female mice fed CFAM; however, no effect was seen in males. In wild-type animals, (ω-1)-laurate hydroxylase (CYP2E1) activity, the expression of which has not been shown to be PPARα dependent, was not affected by the CFAM diet. In contrast, stearoyl-CoA desaturase activity was reduced in wild-type mice. CFAM feeding reduced the activities of ACO, CYP2E1, and stearoyl-CoA desaturase and caused accumulation of lipids in the livers of female PPARα-null mice. These data show that CFAM apparently activate gene expression via the PPARα and have profound effects on lipid homeostasis, exacerbating the disturbances preexisting in mice lacking functional PPARα. Although the data emphasize the importance of PPARα in the metabolism of the CFAM, these results show that PPARα is not the exclusive mediator of the effects of CFAM in lipid metabolism in mice.

Maternal n-3 polyunsaturated fatty acid dietary supply modulates microglia lipid content in the offspring

The brain is highly enriched in long chain polyunsaturated fatty acids (LC-PUFAs) that are esterified into phospholipids, the major components of cell membranes. They accumulate during the perinatal period when the brain is rapidly developing. Hence, the levels of LC-PUFAs in the brains of the offspring greatly depend on maternal dietary intake. Perinatal n-3 PUFA consumption has been suggested to modulate the activity of microglial cells, the brains innate immune cells which contribute to the shaping of neuronal network during development. However, the impact of maternal n-3 PUFA intake on microglial lipid composition in the offspring has never been studied. To investigate the impact of maternal dietary n-3 PUFA supply on microglia lipid composition, pregnant mice were fed with n-3 PUFA deficient, n-3 PUFA balanced or n-3 PUFA supplemented diets during gestation and lactation. At weaning, microglia were isolated from the pups brains to analyze their fatty acid composition and phospholipid class levels. We here report that post-natal microglial cells displayed a distinctive lipid profile as they contained high levels of eicosapentaenoic acid (EPA), more EPA than docosahexaenoic acid (DHA) and large amount of phosphatidylinositol (PI) / phosphatidylserine (PS). Maternal n-3 PUFA supply increased DHA levels and decreased n-6 docosapentaenoic acid (DPA) levels whereas the PI/PS membrane content was inversely correlated to the quantity of PUFAs in the diet. These results raise the possibility of modulating microglial lipid profile and their subsequent activity in the developing brain.