Journal
METABOLISM-CLINICAL AND EXPERIMENTAL
Volume 64, Issue 2, Pages 172-181Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.metabol.2014.10.002
Keywords
Insulin; Adiponectin; Leptin; Airway hyperreactivity
Categories
Funding
- INCT-Obesidade e Diabetes and Research, Innovation and Dissemination Centers (CEPID) - Conselho Nacional de Pesquisa (CNPq)
- INCT-Obesidade e Diabetes and Research, Innovation and Dissemination Centers (CEPID) - Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
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Obesity is a major risk factor for asthma. Likewise, obesity is known to increase disease severity in asthmatic subjects and also to impair the efficacy of first-line treatment medications for asthma, worsening asthma control in obese patients. This concept is in agreement with the current understanding that some asthma phenotypes are not accompanied by detectable inflammation, and may not be ameliorated by classical anti-inflammatory therapy. There are growing evidences suggesting that the obesity-related asthma phenotype does not necessarily involve the classical T(H)2-dependent inflammatory process. Hormones involved in glucose homeostasis and in the pathogeneses of obesity likely directly or indirectly link obesity and asthma through inflammatory and noninflammatory pathways. Furthermore, the endocrine regulation of the airway-related preganglionic nerves likely contributes to airway hyperreactivity (AHR) in obese states. In this review, we focused our efforts on understanding the mechanism underlying obesity-related asthma by exploring the T(H)2-independent mechanisms leading to this disease. (C) 2015 Elsevier Inc. All rights reserved.
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