Oral l-Arginine Stimulates GLP-1 Secretion to Improve Glucose Tolerance in Male Mice

Pharmacological and surgical interventions that increase glucagon-like peptide 1 (GLP-1) action are effective to improve glucose homeostasis in type 2 diabetes mellitus. In light of this, nutritional strategies to enhance postprandial GLP-1 secretion, particularly in the context of diet-induced obes...

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Veröffentlicht in:Endocrinology (Philadelphia) 2013-11, Vol.154 (11), p.3978-3983
Hauptverfasser: Clemmensen, Christoffer, Smajilovic, Sanela, Smith, Eric P, Woods, Stephen C, Bräuner-Osborne, Hans, Seeley, Randy J, D'Alessio, David A, Ryan, Karen K
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container_end_page 3983
container_issue 11
container_start_page 3978
container_title Endocrinology (Philadelphia)
container_volume 154
creator Clemmensen, Christoffer
Smajilovic, Sanela
Smith, Eric P
Woods, Stephen C
Bräuner-Osborne, Hans
Seeley, Randy J
D'Alessio, David A
Ryan, Karen K
description Pharmacological and surgical interventions that increase glucagon-like peptide 1 (GLP-1) action are effective to improve glucose homeostasis in type 2 diabetes mellitus. In light of this, nutritional strategies to enhance postprandial GLP-1 secretion, particularly in the context of diet-induced obesity, may provide an alternative therapeutic approach. Importantly, recent evidence suggests the amino acid l-arginine, a well-known insulin secretagogue, can also stimulate release of GLP-1 from isolated rat intestine. Here we tested the hypothesis that oral l-arginine acts as a GLP-1 secretagogue in vivo, to augment postprandial insulin secretion and improve glucose tolerance. To test this, we administered l-arginine or vehicle by oral gavage, immediately prior to an oral glucose tolerance test in lean and diet-induced obese mice. In both lean and obese mice oral l-arginine increased plasma GLP-1 and insulin and substantially improved glucose clearance. To directly assess the contribution of GLP-1 receptor (GLP-1R)-signaling to these improvements, l-arginine was given to Glp1r knockout mice and their wild-type littermates. In this experiment oral l-arginine significantly augmented insulin secretion and improved glucose clearance in WT mice, but not in Glp1r knockout littermates. Taken together these findings identify l-arginine as a GLP-1 secretagogue in vivo and demonstrate that improvement of glucose tolerance by oral l-arginine depends on GLP-1R-signaling. These findings raise the intriguing possibility that l-arginine-based nutritional and/or pharmaceutical therapies may benefit glucose tolerance by improving the postprandial GLP-1 response in obese individuals.
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In light of this, nutritional strategies to enhance postprandial GLP-1 secretion, particularly in the context of diet-induced obesity, may provide an alternative therapeutic approach. Importantly, recent evidence suggests the amino acid l-arginine, a well-known insulin secretagogue, can also stimulate release of GLP-1 from isolated rat intestine. Here we tested the hypothesis that oral l-arginine acts as a GLP-1 secretagogue in vivo, to augment postprandial insulin secretion and improve glucose tolerance. To test this, we administered l-arginine or vehicle by oral gavage, immediately prior to an oral glucose tolerance test in lean and diet-induced obese mice. In both lean and obese mice oral l-arginine increased plasma GLP-1 and insulin and substantially improved glucose clearance. To directly assess the contribution of GLP-1 receptor (GLP-1R)-signaling to these improvements, l-arginine was given to Glp1r knockout mice and their wild-type littermates. 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In this experiment oral l-arginine significantly augmented insulin secretion and improved glucose clearance in WT mice, but not in Glp1r knockout littermates. Taken together these findings identify l-arginine as a GLP-1 secretagogue in vivo and demonstrate that improvement of glucose tolerance by oral l-arginine depends on GLP-1R-signaling. These findings raise the intriguing possibility that l-arginine-based nutritional and/or pharmaceutical therapies may benefit glucose tolerance by improving the postprandial GLP-1 response in obese individuals.</abstract><cop>Chevy Chase, MD</cop><pub>Endocrine Society</pub><pmid>23959939</pmid><doi>10.1210/en.2013-1529</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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subjects Amino acids
Animals
Arginine
Arginine - pharmacology
Biological and medical sciences
Brief Research Reports
Clearances
Diabetes mellitus
Diabetes mellitus (non-insulin dependent)
Diet
Dietary Fats - pharmacology
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation - drug effects
Glucagon
Glucagon-like peptide 1
Glucagon-Like Peptide 1 - genetics
Glucagon-Like Peptide 1 - metabolism
Glucagon-Like Peptide-1 Receptor
Glucose
Glucose Intolerance - drug therapy
Glucose tolerance
Glucose Tolerance Test
Homeostasis
In vivo methods and tests
Insulin
Insulin - blood
Insulin secretion
Intestine
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Obesity
Obesity - chemically induced
Obesity - metabolism
Receptors, Glucagon - genetics
Receptors, Glucagon - metabolism
Vertebrates: endocrinology
title Oral l-Arginine Stimulates GLP-1 Secretion to Improve Glucose Tolerance in Male Mice
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