Identification of nesfatin-1 as a satiety molecule in the hypothalamus View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2006-10

AUTHORS

Shinsuke Oh-I, Hiroyuki Shimizu, Tetsurou Satoh, Shuichi Okada, Sachika Adachi, Kinji Inoue, Hiroshi Eguchi, Masanori Yamamoto, Toshihiro Imaki, Koushi Hashimoto, Takafumi Tsuchiya, Tsuyoshi Monden, Kazuhiko Horiguchi, Masanobu Yamada, Masatomo Mori

ABSTRACT

The brain hypothalamus contains certain secreted molecules that are important in regulating feeding behaviour. Here we show that nesfatin, corresponding to NEFA/nucleobindin2 (NUCB2), a secreted protein of unknown function, is expressed in the appetite-control hypothalamic nuclei in rats. Intracerebroventricular (i.c.v.) injection of NUCB2 reduces feeding. Rat cerebrospinal fluid contains nesfatin-1, an amino-terminal fragment derived from NUCB2, and its expression is decreased in the hypothalamic paraventricular nucleus under starved conditions. I.c.v. injection of nesfatin-1 decreases food intake in a dose-dependent manner, whereas injection of an antibody neutralizing nesfatin-1 stimulates appetite. In contrast, i.c.v. injection of other possible fragments processed from NUCB2 does not promote satiety, and conversion of NUCB2 to nesfatin-1 is necessary to induce feeding suppression. Chronic i.c.v. injection of nesfatin-1 reduces body weight, whereas rats gain body weight after chronic i.c.v. injection of antisense morpholino oligonucleotide against the gene encoding NUCB2. Nesfatin-1-induced anorexia occurs in Zucker rats with a leptin receptor mutation, and an anti-nesfatin-1 antibody does not block leptin-induced anorexia. In contrast, central injection of alpha-melanocyte-stimulating hormone elevates NUCB2 gene expression in the paraventricular nucleus, and satiety by nesfatin-1 is abolished by an antagonist of the melanocortin-3/4 receptor. We identify nesfatin-1 as a satiety molecule that is associated with melanocortin signalling in the hypothalamus. More... »

PAGES

709

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature05162

DOI

http://dx.doi.org/10.1038/nature05162

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1045417860

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17036007


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