| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8537009 | Pharmacology & Therapeutics | 2017 | 5 Pages |
Abstract
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.
Keywords
NOSRAGEGLP-1RGLP-1HMGB-1pKaAGEsTh1Th2DPP-4ADMANF-κBcAMPMAPKCyclic adenosine monophosphateArginineAsthmainterleukintumor necrosis factor alphaasymmetric dimethylargininedipeptidyl peptidase 4TNF-αnuclear factor kappa-light-chain-enhancer of activated B cellsAdvanced glycation end productsObesityNitric oxidenitric oxide synthaseHigh mobility group box 1 proteinprotein kinase Amitogen-activated protein kinaseglucagon-like peptide 1Receptor for advanced glycation end productsglucagon-like peptide 1 receptor
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Authors
Dan-Vinh Nguyen, Angela Linderholm, Angela Haczku, Nicholas Kenyon,