Obesity and asthma: Possible mechanisms

被引:342
|
作者
Shore, Stephanie A. [1 ]
机构
[1] Harvard Univ, Sch Publ Hlth, Program Mol & Integrat Physiol Sci, Dept Environm Hlth, Boston, MA 02115 USA
关键词
functional residual capacity; airway closure; leptin; adiponectin; macrophage;
D O I
10.1016/j.jaci.2008.03.004
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:1087 / 1093
页数:7
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