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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2009-1-29
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pubmed:abstractText |
Nesfatin-1 is a novel satiety molecule in the hypothalamus and is also present in peripheral tissues. Here we sought to identify the active segment of nesfatin-1 and to determine the mechanisms of its action after peripheral administration in mice. Intraperitoneal injection of nesfatin-1 suppressed food intake in a dose-dependent manner. Nesfatin-1 has three distinct segments; we tested the effect of each segment on food intake. Injection of the midsegment decreased food intake under leptin-resistant conditions such as db/db mice and mice fed a high-fat diet. After injection of the midsegment, expression of c-Fos was significantly activated in the brainstem nucleus tractus solitarius (NTS) but not in the hypothalamic arcuate nucleus; the nicotinic cholinergic pathway to the NTS contributed to midsegment-induced anorexia. Midsegment injection significantly increased expression of proopiomelanocortin and cocaine- and amphetamine-regulated transcript genes in the NTS but not in the arcuate nucleus. Investigation of mutant midsegments demonstrated that a region with amino acid sequence similarity to the active site of agouti-related peptide was indispensable for anorexigenic induction. Our findings indicate that the midsegment of nesfatin-1 causes anorexia, possibly by activating POMC and CART neurons in the NTS via a leptin-independent mechanism after peripheral stimulation.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1945-7170
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pubmed:author |
pubmed-author:EguchiHH,
pubmed-author:HashimotoKK,
pubmed-author:InoueKK,
pubmed-author:KatzDD,
pubmed-author:MoriMM,
pubmed-author:NakataMM,
pubmed-author:Oh-ISS,
pubmed-author:OkadaSS,
pubmed-author:SatohTT,
pubmed-author:ShimizuHH,
pubmed-author:YadaTT,
pubmed-author:YamadaMM,
pubmed-author:YamamotoSS,
pubmed-author:YoshidaNN
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pubmed:issnType |
Electronic
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pubmed:volume |
150
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
662-71
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pubmed:meshHeading |
pubmed-meshheading:19176321-Animals,
pubmed-meshheading:19176321-Anorexia,
pubmed-meshheading:19176321-Arcuate Nucleus,
pubmed-meshheading:19176321-Conditioning (Psychology),
pubmed-meshheading:19176321-Diabetes Mellitus, Experimental,
pubmed-meshheading:19176321-Down-Regulation,
pubmed-meshheading:19176321-Eating,
pubmed-meshheading:19176321-Injections, Intraperitoneal,
pubmed-meshheading:19176321-Leptin,
pubmed-meshheading:19176321-Male,
pubmed-meshheading:19176321-Mice,
pubmed-meshheading:19176321-Mice, Inbred ICR,
pubmed-meshheading:19176321-Nerve Tissue Proteins,
pubmed-meshheading:19176321-Pro-Opiomelanocortin,
pubmed-meshheading:19176321-Protein Structure, Tertiary,
pubmed-meshheading:19176321-Proto-Oncogene Proteins c-fos,
pubmed-meshheading:19176321-Signal Transduction,
pubmed-meshheading:19176321-Solitary Nucleus,
pubmed-meshheading:19176321-Taste
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pubmed:year |
2009
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pubmed:articleTitle |
Peripheral administration of nesfatin-1 reduces food intake in mice: the leptin-independent mechanism.
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pubmed:affiliation |
Department of Medicine and Molecular Science, Gunma University Graduate School of Medicine, Maebashi, Japan. hshimizu@showa.gunma-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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