Liraglutide Suppresses the Plasma Levels of Active and Des-Acyl Ghrelin Independently of Active Glucagon-Like Peptide-1 Levels in Mice. (13th August 2013)

• Record Type: Journal Article
• Authors: Nonogaki, Katsunori; Suzuki, Marina
• Other Names: Giampietro O. Academic Editor.; Morosini P. Academic Editor.
• Is Part Of: ISRN endocrinology. Volume 2013(2013)
• Publication Date: 2013-08-13
• Subjects: Endocrinology -- Periodicals; Endocrine System Diseases; Endocrinology; Endocrinology; Electronic journals; Periodical; Fulltext; Internet Resources; Periodicals; Periodicals; 616.4
• DOI: 10.1155/2013/184753
• Languages: English
• ISSNs: 2090-4630

Abstract

Abstract : Glucagon-like peptide-1 (GLP-1), an insulinotropic gastrointestinal peptide that is primarily produced by intestinal endocrine L-cells, stimulates satiety. Ghrelin, a hormone that is produced predominantly by the stomach stimulates hunger. There are two forms of ghrelin: active ghrelin and inactive des-acyl ghrelin. After depriving mice of food for 24 h, we demonstrated that the systemic administration of liraglutide (100 μ g/kg), a human GLP-1 analog that binds to the GLP-1 receptor, increased (1.4-fold) the plasma levels of active GLP-1 and suppressed the plasma levels of active and des-acyl ghrelin after 1 h. Despite the elevated plasma levels of active GLP-1 (11-fold), liraglutide had no effect on the plasma levels of active or des-acyl ghrelin after 12 h. These findings demonstrated that liraglutide suppresses the plasma levels of active and des-acyl ghrelin independently of active GLP-1 levels in fasted mice, suggesting a novel in vivo biological effect of liraglutide beyond regulating plasma GLP-1.