Department of Food and Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.
Richardson Centre for Functional Foods and Nutraceuticals (RCFFN), University of Manitoba, Winnipeg, Manitoba, Canada.
Obes Rev. 2018 Feb;19(2):178-197. doi: 10.1111/obr.12630. Epub 2017 Nov 10.
Fatty acid ethanolamides are lipid mediators that regulate a plethora of physiological functions. One such bioactive lipid mediator, oleoylethanolamide (OEA), is a potent agonist of the peroxisome proliferator-activated receptor-alpha (PPAR-α), which modulates increased expression of the fatty acid translocase CD36 that enables the regulation of feeding behaviour. Consumption of dietary fat rich in oleic acid activates taste receptors in the gut activating specific enzymes that lead to the formation of OEA. OEA further combines with PPAR-α to enable fat oxidation in the liver, resulting in enhanced energy production. Evidence suggests that sustained ingestion of a high-fat diet abolishes the anorexic signal of OEA. Additionally, malfunction of the enterocyte that transforms oleic acid produced during fat digestion into OEA might be responsible for reduced satiety and hyperphagia, resulting in overweight and obesity. Thus, OEA anorectic signalling may be an essential element of the physiology and metabolic system regulating dietary fat intake and obesity. The evidence reviewed in this article indicates that intake of oleic acid, and thereby the resulting OEA imparting anorexic properties, is dependent on CD36, PPAR-α, enterocyte fat sensory receptors, histamine, oxytocin and dopamine; leading to increased fat oxidation and enhanced energy expenditure to induce satiety and increase feeding latency; and that a disruption in any of these systems will cease/curb fat-induced satiety.
脂肪酸乙醇酰胺是调节多种生理功能的脂质介质。其中一种生物活性脂质介质,油酰乙醇酰胺(OEA),是过氧化物酶体增殖物激活受体-α(PPAR-α)的有效激动剂,可调节脂肪酸转运蛋白 CD36 的表达增加,从而调节摄食行为。富含油酸的饮食中的脂肪被消耗会激活肠道中的味觉感受器,激活特定的酶,导致 OEA 的形成。OEA 进一步与 PPAR-α 结合,使肝脏中的脂肪氧化,从而增加能量产生。有证据表明,持续摄入高脂肪饮食会消除 OEA 的厌食信号。此外,消化脂肪过程中产生的油酸转化为 OEA 的肠细胞功能障碍可能导致饱腹感降低和多食,导致超重和肥胖。因此,OEA 的厌食信号可能是调节饮食脂肪摄入和肥胖的生理和代谢系统的一个重要组成部分。本文综述的证据表明,油酸的摄入,以及由此产生的具有厌食特性的 OEA,依赖于 CD36、PPAR-α、肠细胞脂肪感觉受体、组胺、催产素和多巴胺;导致脂肪氧化增加和能量消耗增加,从而引起饱腹感和增加摄食潜伏期;而这些系统中的任何一个中断/抑制都会导致脂肪诱导的饱腹感丧失。