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

Pharmacol Ther. 2017 Dec:180:139-143. doi: 10.1016/j.pharmthera.2017.06.012. Epub 2017 Jun 22.

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: Advanced glycation end products; Arginine; Asthma; Glucagon-like peptide 1; Obesity.

Publication types

  • Review

MeSH terms

  • 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

Substances

  • Glycation End Products, Advanced
  • Receptor for Advanced Glycation End Products
  • Glucagon-Like Peptide 1
  • Arginine