Jacome-Sosa Miriam, Vacca Claudia, Mangat Rabban, Diane Abdoulaye, Nelson Randy C, Reaney Martin J, Shen Jianheng, Curtis Jonathan M, Vine Donna F, Field Catherine J, Igarashi Miki, Piomelli Daniele, Banni Sebastiano, Proctor Spencer D
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.
Department of Biomedical Sciences, University of Cagliari, Cittadella Universitaria, Monserrato, Cagliari, Italy.
J Lipid Res. 2016 Apr;57(4):638-49. doi: 10.1194/jlr.M066308. Epub 2016 Feb 17.
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.
反式vaccenic酸（VA）是食物链中主要的反刍动物源反式脂肪，可改善高脂血症，但其机制仍不清楚。我们研究了VA是否会通过改变膜磷脂（PL）中生物合成前体花生四烯酸（AA）的可用性来影响组织内源性大麻素（EC）。将JCR：LA-cp大鼠分为对照组，分别给予含或不含VA（1% w/w）、顺式-9，反式-11共轭亚油酸（CLA）（1% w/w）或VA+CLA（1% + 0.5% w/w）的饮食，持续8周。与对照饮食相比，VA降低了肝脏和内脏脂肪组织（VAT）中的EC 2-花生四烯酸甘油酯（2-AG）（P<0.001），但未改变组织PL中的AA。相对于单独使用VA，VA+CLA联合使用对2-AG没有相加作用（P>0.05）。有趣的是，与对照饮食相比，VA增加了空肠中花生四烯乙醇胺的浓度以及非大麻素信号分子油酰乙醇胺和棕榈酰乙醇胺的浓度（P<0.05）。这与它们降解酶脂肪酸酰胺水解酶的空肠蛋白丰度较低（但活性未降低）以及TNFα和白细胞介素1β的mRNA表达一致（P<0.05）。VA降低肝脏和VAT中2-AG的能力为减轻异位脂质积累提供了潜在的机制解释。VA对EC和其他非大麻素脂质信号分子的相反调节表明通过肠道中的EC系统激活了益处。
