Feeding regulation by oleoylethanolamide synthesized from dietary oleic acid
Feeding regulation by oleoylethanolamide synthesized from dietary oleic acid
复制标题
DOI：
10.1016/j.plefa.2020.102228
复制
发表时间：
2021-02-01
影响因子：
3
通讯作者：
Yoshikawa, Keisuke
中科院分区：
文献类型：
--
作者：
Igarashi, Miki;Iwasa, Kensuke;Yoshikawa, Keisuke
油酰乙醇胺（OEA）是一种众所周知的饱腹感因子，在近端肠道进食期间产生。肠细胞通过CD 36感知脂肪中的油酸，并通过NAPE-PLD依赖或独立的途径将其转化为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型（PPAR-alpha）。OEA刺激传入感觉纤维（可能是迷走神经的那些），并引起大脑中使用催产素和组胺作为神经递质来调节饱腹感的进食控制回路的募集。高脂喂养引起的OEA合成功能障碍可能导致体重增加和肥胖。在这里，我们描述了OEA在能量代谢和食物摄入的调节中所发挥的作用，通过介绍我们的初步数据，这种脂质介质，我们简要概述了OEA的生物合成和失活。
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-alpha (PPAR-alpha). 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.