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

被引:39
作者
Dan-Vinh Nguyen [1 ]
Linderholm, Angela [1 ]
Haczku, Angela [1 ]
Kenyon, Nicholas [1 ]
机构
[1] Univ Calif Davis, Vet Affairs Northern Calif Healthcare Syst, Davis, CA 95616 USA
基金
美国国家卫生研究院;
关键词
Glucagon-like peptide 1; Advanced glycation end products; Arginine; Obesity; Asthma; GLYCATION END-PRODUCTS; AIRWAY INFLAMMATION; METABOLIC SYNDROME; ASYMMETRIC DIMETHYLARGININE; DIPEPTIDYL PEPTIDASE-4; RECEPTOR; GLP-1; SECRETION; CELLS; RAGE;
D O I
10.1016/j.pharmthera.2017.06.012
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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. Published by Elsevier Inc.
引用
收藏
页码:139 / 143
页数:5
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