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L-arginine promotes gut hormone release and reduces food intake in rodents

Research output: Contribution to journalArticle

A. Alamshah, A. K. Mcgavigan, E. Spreckley, J. S. Kinsey-Jones, A. Amin, I. R. Tough, H. C. O'Hara, A. Moolla, K. Banks, R. France, G. Hyberg, M. Norton, W. Cheong, A. Lehmann, S. R. Bloom, H. M. Cox, K. G. Murphy

Original languageEnglish
Pages (from-to)508-518
Number of pages11
JournalDIABETES OBESITY AND METABOLISM
Volume18
Issue number5
Early online date11 Feb 2016
DOIs
Publication statusPublished - May 2016

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Abstract

Aims: To investigate the anorectic effect of L-arginine (L-Arg) in rodents. Methods: We investigated the effects of L-Arg on food intake, and the role of the anorectic gut hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), the G-protein-coupled receptor family C group 6 member A (GPRC6A) and the vagus nerve in mediating these effects in rodents. Results: Oral gavage of L-Arg reduced food intake in rodents, and chronically reduced cumulative food intake in diet-induced obese mice. Lack of the GPRC6A in mice and subdiaphragmatic vagal deafferentation in rats did not influence these anorectic effects. L-Arg stimulated GLP-1 and PYY release in vitro and in vivo. Pharmacological blockade of GLP-1 and PYY receptors did not influence the anorectic effect of L-Arg. L-Arg-mediated PYY release modulated net ion transport across the gut mucosa. Intracerebroventricular (i.c.v.) and intraperitoneal (i.p.) administration of L-Arg suppressed food intake in rats. Conclusions: L-Arg reduced food intake and stimulated gut hormone release in rodents. The anorectic effect of L-Arg is unlikely to be mediated by GLP-1 and PYY, does not require GPRC6A signalling and is not mediated via the vagus. I.c.v. and i.p. administration of L-Arg suppressed food intake in rats, suggesting that L-Arg may act on the brain to influence food intake. Further work is required to determine the mechanisms by which L-Arg suppresses food intake and its utility in the treatment of obesity.

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