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Central and peripheral des-acyl ghrelin regulates body temperature in rats
Authors:Yoshiyuki Inoue  Keiko Nakahara  Keisuke Maruyama  Yoshiharu Suzuki  Yujiro Hayashi  Kenji Kangawa  Noboru Murakami
Institution:1. Department of Pathophysiological Laboratory Science, Nagoya University Graduate School of Medicine, Nagoya, Japan;2. College of Life and Health Sciences, Chubu University, Kasugai, Japan;3. Department of Molecular and Cellular Pathophysiology and Therapeutics, Graduate School of Pharmaceutical Science, Nagoya City University, Nagoya, Japan;4. Equipment Center for Research and Education, Nagoya University Graduate School of Medicine, Nagoya, Japan;5. Department of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan;6. Division of Molecular Carcinogenesis, Nagoya University Graduate School of Medicine, Nagoya, Japan;7. Department of Drug Information, Gifu Pharmaceutical University, Gifu, Japan;8. Department of Dermatology, Gifu Graduate School of Medicine, Gifu, Japan;9. Tokai Gakuin University, Kakamigahara, Japan;1. Department of Cardiology, Osaka City General Hospital, Osaka 534–0021, Japan;2. Department of Pathology, Osaka City General Hospital, Osaka 534–0021, Japan;3. Department of Cardiology and Internal Medicine, Osaka City University Graduate School of Medicine, Osaka 545-8585, Japan;4. Department of Pathology, Osaka City University Graduate School of Medicine, Osaka 545-8585, Japan;5. Academic Medical Center, University of Amsterdam, Amsterdam 1105, AZ The Netherlands;1. Department of Dermatology, University of Occupational and Environmental Health, Kitakyushu, Japan;2. Department of Dermatology, Hamamatsu University School of Medicine, Hamamatsu, Japan
Abstract:In the present study using rats, we demonstrated that central and peripheral administration of des-acyl ghrelin induced a decrease in the surface temperature of the back, and an increase in the surface temperature of the tail, although the effect of peripheral administration was less marked than that of central administration. Furthermore, these effects of centrally administered des-acyl ghrelin could not be prevented by pretreatment with D-Lys3]-GHRP-6 GH secretagogue receptor 1a (GHS-R1a) antagonists. Moreover, these actions of des-acyl ghrelin on body temperature were inhibited by the parasympathetic nerve blocker methylscopolamine but not by the sympathetic nerve blocker timolol. Using immunohistochemistry, we confirmed that des-acyl ghrelin induced an increase of cFos expression in the median preoptic nucleus (MnPO). Additionally, we found that des-acyl ghrelin dilated the aorta and tail artery in vitro. These results indicate that centrally administered des-acyl ghrelin regulates body temperature via the parasympathetic nervous system by activating neurons in the MnPO through interactions with a specific receptor distinct from the GHS-R1a, and that peripherally administered des-acyl ghrelin acts on the central nervous system by passing through the blood–brain barrier, whereas it exerts a direct action on the peripheral vascular system.
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