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This version published online on February 17, 2005
Endocrinology, doi:10.1210/en.2004-1266
A more recent version of this article appeared on May 1, 2005
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Submitted on September 24, 2004
Accepted on February 7, 2005

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

SHUICHI KODA, YUKARI DATE, NOBORU MURAKAMI, TAKUYA SHIMBARA, TAKESHI HANADA, KOJI TOSHINAI, AKIRA NIIJI MA, MAYUMI FURUYA, NORIO INOMATA, KAZUHIRO OSUYE, and MASAMITSU NAKAZATO*

Third Department of Internal Medicine (S.K., Y.D., T.S., T.H., K.T., M.N.), Miyazaki Medical College, University of Miyazaki, Miyazaki 889-1692, Japan; Daiichi Suntory Biomedical Research Co., Ltd. (S.K., M.F., N.I.), Osaka 681-8513, Japan; Department of Veterinary Physiology (N.M.), Faculty of Agriculture, Miyazaki University, Miyazaki 889-2192, Japan; Department of Physiology, Niigata University School of Medicine (A.N.), Niigata 951-8510, Japan; and Daiichi Suntory Pharma Co., Ltd. (T.H., K.O.), Gunma 370-0503, Japan

* To whom correspondence should be addressed. E-mail: nakazato{at}med.miyazaki-u.ac.jp.

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 NPY 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 via 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 intravenously. 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 (NTS) on the transmission of PYY3-36-mediated satiety signals. In rats, bilateral midbrain transections rostral to the NTS 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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