Rapeseed Lecithin Increases Lymphatic Lipid Output and α-Linolenic Acid Bioavailability in Rats

Author:

Robert Chloé12,Couëdelo Leslie2ORCID,Knibbe Carole13ORCID,Fonseca Laurence2,Buisson Charline1,Errazuriz-Cerda Elisabeth4,Meugnier Emmanuelle1,Loizon Emmanuelle1,Vaysse Carole2ORCID,Michalski Marie-Caroline1ORCID

Affiliation:

1. Univ-Lyon, CarMeN (Cardiovascular, Metabolism, Diabetes, Nutrition) Laboratory, National Institute for Agricultural and Environmental Research (INRAE) UMR1397, National Institute of Health and Medical Research (INSERM) U1060, National Institute of Applied Science of Lyon (INSA-Lyon), Université Claude Bernard Lyon 1, Pierre-Bénite, France

2. ITERG, Equipe Nutrition, Santé et Biochimie des Lipides, Canéjan, France

3. Inria “Beagle” team, Antenne Lyon la Doua, Villeurbanne, France

4. Center of Quantitative Imagery Lyon Est (CIQLE), Université Claude Bernard Lyon 1, Lyon, France

Abstract

ABSTRACTBackgroundSoybean lecithin, a plant-based emulsifier widely used in food, is capable of modulating postprandial lipid metabolism. With arising concerns of sustainability, alternative sources of vegetal lecithin are urgently needed, and their metabolic effects must be characterized.ObjectivesWe evaluated the impact of increasing doses of rapeseed lecithin (RL), rich in essential α-linolenic acid (ALA), on postprandial lipid metabolism and ALA bioavailability in lymph-cannulated rats.MethodsMale Wistar rats (8 weeks old) undergoing a mesenteric lymph duct cannulation were intragastrically administered 1 g of an oil mixture containing 4% ALA and 0, 1, 3, 10, or 30% RL (5 groups). Lymph fractions were collected for 6 h. Lymph lipids and chylomicrons (CMs) were characterized. The expression of genes implicated in intestinal lipid metabolism was determined in the duodenum at 6 h. Data was analyzed using either sigmoidal or linear mixed-effects models, or one-way ANOVA, where appropriate.ResultsRL dose-dependently increased the lymphatic recovery (AUC) of total lipids (1100 μg/mL·h per additional RL%; P = 0.010) and ALA (50 μg/mL·h per additional RL%; P = 0.0076). RL induced a faster appearance of ALA in lymph, as evidenced by the exponential decrease of the rate of appearance of ALA with RL (R2 = 0.26; P = 0.0064). Although the number of CMs was unaffected by RL, CM diameter was increased in the 30%-RL group, compared to the control group (0% RL), by 86% at 3–4 h (P = 0.065) and by 81% at 4–6 h (P = 0.0002) following administration. This increase was positively correlated with the duodenal mRNA expression of microsomal triglyceride transfer protein (Mttp; ρ= 0.63; P = 0.0052). The expression of Mttp and secretion-associated, ras-related GTPase 1 gene homolog B (Sar1b, CM secretion), carnitine palmitoyltransferase IA (Cpt1a) and acyl-coenzyme A oxidase 1 (Acox1, beta-oxidation), and fatty acid desaturase 2 (Fads2, bioconversion of ALA into long-chain n–3 PUFAs) were, respectively, 49%, 29%, 74%, 48%, and 55% higher in the 30%-RL group vs. the control group (P < 0.05).ConclusionsIn rats, RL enhanced lymphatic lipid output, as well as the rate of appearance of ALA, which may promote its subsequent bioavailability and metabolic fate.

Funder

Région Nouvelle Aquitain

FEDER

Publisher

Oxford University Press (OUP)

Subject

Nutrition and Dietetics,Medicine (miscellaneous)

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