期刊
PEPTIDES
卷 30, 期 12, 页码 2228-2232出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.peptides.2009.08.018
关键词
Food intake; beta-Lactotensin; Neurotensin; Calcitonin gene-related peptide; Corticotropin releasing factor
资金
- Japanese Society for the Promotion of Science
- Japan Dairy Association
We found that beta-lactotensin (His-Ile-Arg-Leu), which has been isolated as an ileum-contracting peptide from chymotrypsin digest of bovine beta-lactoglobulin, dose-dependently suppresses food intake after intracerebroventricular (i.c.v.) or intraperitoneal administration at a dose of 40 nmol/mouse or 100 mg/kg, respectively, in fasted mice. Orally administered beta-lactotensin also suppressed food intake at 500 mg/kg. We previously reported that beta-lactotensin acts as an agonist for neurotensin receptors; however, the anorexigenic activity of beta-lactotensin was not inhibited by i.c.v. co-administration with SR48692 or levocabastine, an antagonist for neurotensin NT, or NT2 receptor, respectively. On the other hand, the anorexigenic effect of beta-lactotensin was blocked by i.c.v. co-administration with astressin or calcitonin gene-related peptide (CGRP)(8-37), an antagonist for corticotropin releasing factor (CRF) or CGRP, respectively. beta-Lactotensin had affinity for neither CRF nor CGRP receptor. In addition, CRF-induced anorexigenic activity after i.c.v. administration was completely blocked by CGRP(8-37), while CGRP-induced anorexigenic activity was not inhibited by astressin. These results suggest that the CGRP system is activated downstream of the CRF system in food intake regulation. Taken together, beta-lactotensin may suppress food intake by activating the CRF system followed by the CGRP system, independently of the neurotensin system. (C) 2009 Elsevier Inc. All rights reserved.
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