L-Arginine promotes gut hormone release and reduces food intake in rodents
File(s)
Published version
Accepted version
Author(s)
Type
Journal Article
Abstract
Aims
The amino acids generated by protein digestion may play a role in the weight loss driven by high protein diets. We investigated the anorectic effect of L-arginine (L-Arg) in rodents.
Materials and Methods
We investigated the effect 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 or 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 (ICV) and intraperitoneal (IP) 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. ICV and IP administration of L-Arg suppressed food intake in rats, suggesting that L-Arg may act upon 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.
The amino acids generated by protein digestion may play a role in the weight loss driven by high protein diets. We investigated the anorectic effect of L-arginine (L-Arg) in rodents.
Materials and Methods
We investigated the effect 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 or 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 (ICV) and intraperitoneal (IP) 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. ICV and IP administration of L-Arg suppressed food intake in rats, suggesting that L-Arg may act upon 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.
Date Issued
2016-02-11
Date Acceptance
2016-02-07
Citation
Diabetes Obesity & Metabolism, 2016, 18 (5), pp.508-518
ISSN
1463-1326
Publisher
Wiley
Start Page
508
End Page
518
Journal / Book Title
Diabetes Obesity & Metabolism
Volume
18
Issue
5
License URL
Sponsor
Biotechnology and Biological Sciences Research Council (BBSRC)
Medical Research Council (MRC)
NC3Rs (National Centre for the Replacement, Refinement and Reduction of Animals in Research)
Technology Strategy Board
Grant Number
BB/I001816/1
MR/J010944/1
NC/K500379/1
101127
Subjects
GLP-1
animal pharmacology
body composition
energy regulation
obesity therapy
Endocrinology & Metabolism
1103 Clinical Sciences
Publication Status
Published