期刊
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
卷 121, 期 5, 页码 1087-1093出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2008.03.004
关键词
functional residual capacity; airway closure; leptin; adiponectin; macrophage
资金
- NHLBI NIH HHS [HL-084044, R01 HL084044] Funding Source: Medline
- NIEHS NIH HHS [ES-00002, ES-013307] Funding Source: Medline
Epidemiologic data indicate that obesity increases the prevalence and incidence of asthma and reduces asthma control. Obese mice exhibit innate airway hyperresponsiveness and augmented responses to certain asthma triggers, further supporting a relationship between obesity and asthma. Here I discuss several mechanisms that may explain this relationship. In obesity, lung volume and tidal volume are reduced, events that promote airway narrowing. Obesity also leads to a state of low-grade systemic inflammation that may act on the lung to exacerbate asthma. Obesity-related changes in adipose-derived hormones, including leptin and adiponectin, may participate in these events. Comorbidities of obesity, such as dyslipidemia, gastroesophageal reflux, sleep-disordered breathing, type 2 diabetes, or hypertension may provoke or worsen asthma. Finally, obesity and asthma may share a common etiology, such as common genetics, common in utero conditions, or common predisposing dietary factors. Novel therapeutic strategies for treatment of the obese patient with asthma may result from an increased understanding of the mechanisms underlying this relationship.
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