A role of nesfatin-1/NucB2 in dehydration-induced anorexia.
Nesfatin-1/NucB2, an anorexigenic molecule, is expressed mainly in the hypothalamus, particularly in the supraoptic nucleus (SON) and the paraventricular nucleus (PVN). Nesfatin-1/NucB2 is also expressed in the subfornical organ (SFO). Because the SON and PVN are involved in body fluid regulation, nesfatin-1/NucB2 may be involved in dehydration-induced anorexia. To clarify the effects of endogenous nesfatin-1/NucB2, we studied changes in nesfatin-1/NucB2 mRNA levels in the SFO, SON, and PVN in adult male Wistar rats after exposure to osmotic stimuli by using in situ hybridization histochemistry. Significant increases in nesfatin-1/NucB2 mRNA levels, ∼2- to 3-fold compared with control, were observed in the SFO, SON, and PVN following water deprivation for 48 h, consumption of 2% NaCl hypertonic saline in drinking water for 5 days, and polyethylene glycol-induced hypovolemia. In addition, nesfatin-1/NucB2 expression was increased in response to water deprivation in a time-dependent manner. These changes in nesfatin-1/NucB2 mRNA expression were positively correlated with plasma sodium concentration, plasma osmolality, and total protein levels in all of the examined nuclei. Immunohistochemistry for nesfatin-1/NucB2 revealed that nesfatin-1/NucB2 protein levels were also increased after 48 h of dehydration and attenuated by 24 h of rehydration. Moreover, intracerebroventricular administration of nesfatin-1/NucB2-neutralizing antibody after 48 h of water deprivation resulted in a significant increase in food intake compared with administration of vehicle alone. These results suggested that nesfatin-1/NucB2 is a crucial peptide in dehydration-induced anorexia.
Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan;
Mitsuhiro
M
Yoshimura
Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan;
Takanori
T
Matsuura
Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan;
Junichi
J
Ohkubo
Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan;
Takashi
T
Maruyama
Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan;
Toru
T
Ishikura
Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan;
Hirofumi
H
Hashimoto
Department of Internal Medicine 1, Faculty of Medicine, Oita University, Oita, Japan; and.
Tetsuya
T
Kakuma
Department of Medicine and Molecular Science, Gunma University, Graduate School of Medicine, Showa-machi, Maebashi, Japan.
Masatomo
M
Mori
Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan; yoichi@med.uoeh-u.ac.jp.
Yoichi
Y
Ueta
D000818:Animals; D000855:Anorexia / Q000209:etiology* / Q000378:metabolism; D002135:Calcium-Binding Proteins / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000378:metabolism*; D003681:Dehydration / Q000150:complications / Q000503:physiopathology*; D004435:Eating / Q000502:physiology; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D000080866:Nucleobindins; D010286:Paraventricular Hypothalamic Nucleus / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000097:blood; D013495:Supraoptic Nucleus / Q000378:metabolism*; D014868:Water Deprivation / Q000502:physiology
D002135:Calcium-Binding Proteins; D004268:DNA-Binding Proteins; D009419:Nerve Tissue Proteins; C000630652:Nucb1 protein, rat; D000080866:Nucleobindins; D012333:RNA, Messenger; D012964:Sodium
anorexia; dehydration; feeding; hypothalamus; nesfatin-1/NucB2