由膳食油酸合成的油酰乙醇酰胺对摄食的调节作用。

Feeding regulation by oleoylethanolamide synthesized from dietary oleic acid.

机构信息

Department of Applied Biological Science, Graduate School of Agriculture, Tokyo University of Agriculture and Technology, Fuchu, Tokyo, Japan.

Department of Pharmacology, Faculty of Medicine, Saitama Medical University, Iruma-gun, Saitama, Japan.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 2021 Feb;165:102228. doi: 10.1016/j.plefa.2020.102228. Epub 2020 Dec 29.

DOI:10.1016/j.plefa.2020.102228

PMID:33385936

Abstract

Oleoylethanolamide (OEA), a well-known satiety factor, is produced during feeding in the proximal intestine. Enterocytes sense oleic acid in dietary fat via CD36 and convert it to OEA through NAPE-PLD dependent or independent pathways. The satiety function of OEA is known to involve peroxisome proliferator-activated receptor type-α (PPAR-α). OEA stimulates afferent sensory fibers (possibly those of the vagus nerve) and provoke the recruitment of feeding-controlling circuits in the brain that use oxytocin and histamine as neurotransmitters for regulating satiety. Dysfunction of OEA synthesis by high-fat feeding might contribute to increased weight and obesity. Here, we describe the roles played by OEA in the regulation of energy metabolism and food intake by introducing our preliminary data regarding this lipid mediator, and we briefly outline the biosynthesis and deactivation of OEA.

摘要

油酰乙醇胺（OEA）是一种众所周知的饱腹感因子，在进食过程中由近端肠道产生。肠细胞通过 CD36 感知膳食脂肪中的油酸，并通过 NAPE-PLD 依赖或非依赖途径将其转化为 OEA。已知 OEA 的饱腹感功能涉及过氧化物酶体增殖物激活受体-α（PPAR-α）。OEA 刺激传入感觉纤维（可能是迷走神经纤维），并募集大脑中控制进食的回路，这些回路使用催产素和组胺作为调节饱腹感的神经递质。高脂肪喂养导致 OEA 合成功能障碍可能导致体重增加和肥胖。在这里，我们通过介绍有关这种脂质介质的初步数据，描述了 OEA 在调节能量代谢和食物摄入中的作用，并简要概述了 OEA 的生物合成和失活。