The Role of the Vagal Nerve in Peripheral PYY3–36-Induced Feeding Reduction in Rats

结节状神经节 孤束 内分泌学 内科学 迷走神经 肽YY 孤核 生长素 胆囊收缩素 背运动核 迷走神经切断术 神经肽 生物 医学 受体 中枢神经系统 神经肽Y受体 激素 刺激
作者
Shuichi Koda,Yukari Date,Noboru Murakami,Takuya Shimbara,Takeshi Hanada,Koji Toshinai,Akira Niijima,Mayumi Furuya,Norio Inomata,Kazuhiro Osuye,Masamitsu Nakazato
出处
期刊:Endocrinology [Oxford University Press]
卷期号:146 (5): 2369-2375 被引量:418
标识
DOI:10.1210/en.2004-1266
摘要

Abstract Peptide YY (PYY), an anorectic peptide, is secreted postprandially from the distal gastrointestinal tract. PYY3–36, the major form of circulating PYY, binds to the hypothalamic neuropeptide Y Y2 receptor (Y2-R) with a high-affinity, reducing food intake in rodents and humans. Additional gastrointestinal hormones involved in feeding, including cholecystokinin, glucagon-like peptide 1, and ghrelin, transmit satiety or hunger signals to the brain via the vagal afferent nerve and/or the blood stream. Here we determined the role of the afferent vagus nerve in PYY function. Abdominal vagotomy abolished the anorectic effect of PYY3–36 in rats. Peripheral administration of PYY3–36 induced Fos expression in the arcuate nucleus of sham-operated rats but not vagotomized rats. We showed that Y2-R is synthesized in the rat nodose ganglion and transported to the vagal afferent terminals. PYY3–36 stimulated firing of the gastric vagal afferent nerve when administered iv. Considering that Y2-R is present in the vagal afferent fibers, PYY3–36 could directly alter the firing rate of the vagal afferent nerve via Y2-R. We also investigated the effect of ascending fibers from the nucleus of the solitary tract on the transmission of PYY3–36-mediated satiety signals. In rats, bilateral midbrain transections rostral to the nucleus of the solitary tract also abolished PYY3–36-induced reductions in feeding. This study indicates that peripheral PYY3–36 may transmit satiety signals to the brain in part via the vagal afferent pathway.
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