Glucagon-like peptide 1: A potential anti-inflammatory pathway in obesity-related asthma

Alterations in arginine metabolism and accelerated formation of advanced glycation end-products (AGEs), crucial mechanisms in obesity-related asthma, can be modulated by glucagon-like peptide 1 (GLP-1). l-arginine dysregulation in obesity promotes inflammation and bronchoconstriction. Prolonged hype...

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Bibliographic Details
Published in:Pharmacology & therapeutics (Oxford) 2017-12, Vol.180, p.139-143
Main Authors: Nguyen, Dan-Vinh, Linderholm, Angela, Haczku, Angela, Kenyon, Nicholas
Format: Article
Language:English
Subjects:
Animals
Arginine - metabolism
Asthma - etiology
Asthma - metabolism
Glucagon-Like Peptide 1 - metabolism
Glycation End Products, Advanced - metabolism
Humans
Inflammation - metabolism
Lung - metabolism
Obesity - complications
Obesity - metabolism
Receptor for Advanced Glycation End Products - metabolism
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Summary:Alterations in arginine metabolism and accelerated formation of advanced glycation end-products (AGEs), crucial mechanisms in obesity-related asthma, can be modulated by glucagon-like peptide 1 (GLP-1). l-arginine dysregulation in obesity promotes inflammation and bronchoconstriction. Prolonged hyperglycemia, dyslipidemia, and oxidative stress leads to production of AGEs, that bind to their receptor (RAGE) further potentiating inflammation. By binding to its widely distributed receptor, GLP-1 blunts the effects of RAGE activation and arginine dysregulation. The GLP-1 pathway, while comprehensively studied in the endocrine and cardiovascular literature, is under-recognized in pulmonary research. Insights into GLP-1 and the lung may lead to novel treatments for obesity-related asthma.
ISSN:0163-7258
1879-016X
DOI:10.1016/j.pharmthera.2017.06.012