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The Role of the Vagal Nerve in Peripheral PYY_3–36-Induced Feeding Reduction in Rats

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; 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; Department of Physiology, Niigata University School of Medicine (A.N.), Niigata 951-8510; and Daiichi Suntory Pharma Co., Ltd. (T.H., K.O.), Gunma 370-0503, Japan

Address all correspondence and requests for reprints to: Masamitsu Nakazato, M.D., Ph.D., Third Department of Internal Medicine, Miyazaki Medical College, University of Miyazaki, Kiyotake, Miyazaki 889-1692, Japan. E-mail: nakazato{at}med.miyazaki-u.ac.jp.

Peptide YY (PYY), an anorectic peptide, is secreted postprandially from the distal gastrointestinal tract. PYY_3–36, 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 PYY_3–36 in rats. Peripheral administration of PYY_3–36 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. PYY_3–36 stimulated firing of the gastric vagal afferent nerve when administered iv. Considering that Y2-R is present in the vagal afferent fibers, PYY_3–36 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 PYY_3–36-mediated satiety signals. In rats, bilateral midbrain transections rostral to the nucleus of the solitary tract also abolished PYY_3–36-induced reductions in feeding. This study indicates that peripheral PYY_3–36 may transmit satiety signals to the brain in part via the vagal afferent pathway.

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