Modulation of plasma N-acylethanolamine levels and physiological parameters by dietary fatty acid composition in humans

Abstract

N-Acylethanolamines (NAEs) are endogenous lipid-signaling molecules involved in satiety and energetics; however, how diet impacts circulating NAE concentrations and their downstream metabolic actions in humans remains unknown. Objectives were to examine effects of diets enriched with high-oleic canola oil (HOCO) or HOCO blended with flaxseed oil (FXCO), compared with a Western diet (WD), on plasma NAE levels and the association with energy expenditure and substrate oxidation. Using a randomized controlled crossover design, 36 hypercholesterolemic participants consumed three isoenergetic diets for 28 days, each containing 36% energy from fat, of which 70% was HOCO, FXCO, or WD. Ultra-performance liquid chromatography-MS/MS was used to measure plasma NAE levels and indirect calorimetry to assess energy expenditure and substrate oxidation. After 28 days, compared with WD, plasma oleoylethanolamide (OEA) and alpha-linolenoyl ethanolamide (ALEA) levels were significantly increased in response to HOCO and FXCO (P = 0.002, P < 0.001), respectively. Correlation analysis demonstrated an inverse association between plasma OEA levels and percent body fat (r = -0.21, P = 0.04), and a positive association was observed between the plasma arachidonoyl ethanolamide (AEA)/OEA ratio and android:gynoid fat (r = 0.23, P = 0.02), respectively. Results suggest that plasma NAE levels are upregulated via their dietary lipid substrates and may modulate regional and total fat mass through lipid-signaling mechanisms.

Trial registration: ClinicalTrials.gov NCT00927199.

Keywords: arachidonoylethanolamide; body composition; canola oil; clinical trials; endocannabinoids; fatty acid metabolism; fatty acid oxidation; oleic acid; oleoylethanolamide; peroxisome proliferator-activated receptor.

Copyright © 2014 by the American Society for Biochemistry and Molecular Biology, Inc.

Figures

Fig. 1.

Selected plasma fatty acid concentrations after consumption of each of the three treatment diets: WD (white bars), FXCO (gray bars), and HOCO (black bars). Values are presented as means ± SEM (n = 36); mean values with different lowercase letters are significantly different between treatment groups (P < 0.05) as analyzed by mixed-model ANOVA (with the Bonferroni adjustment for multiple comparisons). AA, arachidonic acid; OA, oleic acid; PA, palmitic acid.

Fig. 2.

Plasma N-acylethanolamine concentrations after consumption of each of the three treatment diets: WD (white bars), FXCO (gray bars), and HOCO (black bars). Values are presented as means ± SEM (n = 36 for all NAEs, except n = 34 for ALEA); mean values with different lowercase letters are significantly different between treatment groups (P < 0.05) as analyzed by mixed-model ANOVA (with the Bonferroni adjustment for multiple comparisons). ALEA, α-linolenoylethanolamide; DHEA, docosahexaenoylethanolamide; LEA, linoleoylethanolamide.