Dietary fatty acids augment tissue levels of n-acylethanolamines in n-acylphosphatidylethanolamine phospholipase D (NAPE-PLD) knockout mice.

Autor: Lin L; Department of Nutritional Sciences, University of Toronto, Toronto, Canada., Metherel AH; Department of Nutritional Sciences, University of Toronto, Toronto, Canada., Kitson AP; Department of Nutritional Sciences, University of Toronto, Toronto, Canada., Alashmali SM; Department of Nutritional Sciences, University of Toronto, Toronto, Canada., Hopperton KE; Department of Nutritional Sciences, University of Toronto, Toronto, Canada., Trépanier MO; Department of Nutritional Sciences, University of Toronto, Toronto, Canada., Jones PJ; Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Canada., Bazinet RP; Department of Nutritional Sciences, University of Toronto, Toronto, Canada. Electronic address: richard.bazinet@utoronto.ca.
Jazyk: angličtina
Zdroj: The Journal of nutritional biochemistry [J Nutr Biochem] 2018 Dec; Vol. 62, pp. 134-142. Date of Electronic Publication: 2018 Sep 05.
DOI: 10.1016/j.jnutbio.2018.08.015
Abstrakt: N-acylethanolamines (NAEs) are lipid signaling mediators, which can be synthesized from dietary fatty acids via n-acylphosphatidylethanolamine-phospholipase D (NAPE-PLD) and in turn influence physiological outcomes; however, the roles of NAPE-PLD upon dietary fatty acid modulation are not fully understood. Presently, we examine if NAPE-PLD is necessary to increase NAEs in response to dietary fatty acid manipulation. Post-weaning male wild-type (C57Bl/6), NAPE-PLD (-/+) and NAPE-PLD (-/-) mice received isocaloric fat diets containing either beef tallow, corn oil, canola oil or fish oil (10% wt/wt from fat) for 9 weeks. Brain docosahexaenoic acid (DHA) levels were higher (P<.01) in NAPE-PLD (-/+) (10.01±0.31 μmol/g) and NAPE-PLD (-/-) (10.89±0.61 μmol/g) than wild-type (7.72±0.61 μmol/g) consuming fish oil. In NAPE-PLD (-/-) mice, brain docosahexaenoylethanolamide (DHEA) levels were higher (P<.01) after fish oil feeding suggesting that NAPE-PLD was not necessary for DHEA synthesis. Liver and jejunum arachidonoylethanolamide, 1,2-arachidonoylglycerol and DHEA levels reflected their corresponding fatty acid precursors suggesting that alternate pathways are involved in NAE synthesis. NAPE-PLD (-/-) mice had lower oleoylethanolamide levels in the jejunum and a leaner phenotype compared to wild-type mice. Overall, these results demonstrate that dietary fatty acid can augment tissue NAEs in the absence of NAPE-PLD.
(Copyright © 2018 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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