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J Lipid Res. 2016 Apr;57(4):638-49. doi: 10.1194/jlr.M066308. Epub 2016 Feb 17.

Vaccenic acid suppresses intestinal inflammation by increasing anandamide and related N-acylethanolamines in the JCR:LA-cp rat.

Author information

1
Metabolic and Cardiovascular Disease Laboratory, Group on Molecular and Cell Biology of Lipids, Alberta Diabetes and Mazankowski Heart Institutes, University of Alberta, Edmonton, AB, Canada.
2
Department of Biomedical Sciences, University of Cagliari, Cittadella Universitaria, Monserrato, Cagliari, Italy.
3
Department of Plant Science, University of Saskatchewan, Saskatoon, SK, Canada.
4
Department of Agricultural Food and Nutritional Science, University of Alberta, Edmonton, AB, Canada.
5
Laboratory for Medical Homeostasis, RIKEN Center for Integrative Medical Sciences, Kanagawa, Japan.
6
Departments of Anatomy and Neurobiology, Pharmacology, and Biological Chemistry, University of California, Irvine, CA.
7
Metabolic and Cardiovascular Disease Laboratory, Group on Molecular and Cell Biology of Lipids, Alberta Diabetes and Mazankowski Heart Institutes, University of Alberta, Edmonton, AB, Canada spencer.proctor@ualberta.ca.

Abstract

Vaccenic acid (VA), the predominant ruminant-derivedtransfat in the food chain, ameliorates hyperlipidemia, yet mechanisms remain elusive. We investigated whether VA could influence tissue endocannabinoids (ECs) by altering the availability of their biosynthetic precursor, arachidonic acid (AA), in membrane phospholipids (PLs). JCR:LA-cprats were assigned to a control diet with or without VA (1% w/w),cis-9,trans-11 conjugated linoleic acid (CLA) (1% w/w) or VA+CLA (1% + 0.5% w/w) for 8 weeks. VA reduced the EC, 2-arachidonoylglycerol (2-AG), in the liver and visceral adipose tissue (VAT) relative to control diet (P< 0.001), but did not change AA in tissue PLs. There was no additive effect of combining VA+CLA on 2-AG relative to VA alone (P> 0.05). Interestingly, VA increased jejunal concentrations of anandamide and those of the noncannabinoid signaling molecules, oleoylethanolamide and palmitoylethanolamide, relative to control diet (P< 0.05). This was consistent with a lower jejunal protein abundance (but not activity) of their degrading enzyme, fatty acid amide hydrolase, as well as the mRNA expression of TNFα and interleukin 1β (P< 0.05). The ability of VA to reduce 2-AG in the liver and VAT provides a potential mechanistic explanation to alleviate ectopic lipid accumulation. The opposing regulation of ECs and other noncannabinoid lipid signaling molecules by VA suggests an activation of benefit via the EC system in the intestine.

KEYWORDS:

N-acylethanolamines; anandamide; endocannabinoids; intestinal inflammatory diseases; vaccenic acid

PMID:
26891736
PMCID:
PMC4808772
DOI:
10.1194/jlr.M066308
[Indexed for MEDLINE]
Free PMC Article

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