Epidemiological studies indicate the incidence of asthma is increased in obese and overweight humans. Responses to ozone (O(3)), an asthma trigger, are increased in obese (ob/ob) mice lacking the satiety hormone leptin. The long form of leptin receptor (Ob-R(b)) is required for satiety; mice lacking this receptor (db/db mice) are also substantially obese. Here, wild-type (WT) and db/db mice were exposed to air or O(3) (2 ppm) for 3 h. Airway responsiveness, measured by the forced oscillation technique, was greater in db/db than WT mice after air exposure. O(3)-induced increases in pulmonary resistance and airway responsiveness were also greater in db/db mice. BALF eotaxin, IL-6, KC, and MIP-2 increased 4 h after O(3) exposure and subsided by 24 h, whereas protein and neutrophils continued to increase through 24 h. For each outcome, the effect of O(3) was significantly greater in db/db than WT mice. Previously published results obtained in ob/ob mice were similar except for O(3)-induced neutrophils and MIP-2, which were not different from WT mice. O(3) also induced pulmonary IL-1beta and TNF-alpha mRNA expression in db/db but not ob/ob mice. Leptin was increased in serum of db/db mice, and pulmonary mRNA expression of short form of leptin receptor (Ob-R(a)) was similar in db/db and WT mice. These data confirm obese mice have innate airway hyperresponsiveness and increased pulmonary responses to O(3). Differences between ob/ob mice, which lack leptin, and db/db mice, which lack Ob-R(b) but not Ob-R(a), suggest leptin, acting through Ob-R(a), can modify some pulmonary responses to O(3).
"There have also been studies indicating that obese subjects' exposure to higher levels of air pollutants result in higher mortality or morbidity from cardiovascular diseases (Miller et al., 2007; Puett et al., 2009; Weichenthal et al., 2014). Laboratory studies have demonstrated that exposure to higher levels of air pollutants can increase inflammation expressions in bronchoalveolar lavage in obese mice (Johnston et al., 2008; Lu et al., 2006; Shore et al., 2003; Shore et al., 2008). Therefore, populations with higher BMI have higher risk of cardiovascular diseases when they are exposed to higher levels of indoor air pollution than those with lower BMI. "
[Show abstract][Hide abstract] ABSTRACT: This study investigates the effects of high body mass index (BMI) of subjects on individual who exhibited high cardiovascular disease indexes with blood pressure (BP) and heart rate (HR) when exposed to high levels of indoor air pollutants. We collected 115 office workers, and measured their systolic blood pressure (SBP), diastolic blood pressure (DBP) and HR at the end of the workday. The subjects were divided into three groups according to BMI: 18-24 (normal weight), 24-27 (overweight) and >27 (obese). This study also measured the levels of carbon dioxide (CO2), total volatile organic compounds (TVOC), particulate matter with an aerodynamic diameter less than 2.5μm (PM2.5), as well as the bacteria and fungi in the subjects' work-places. The pollutant effects were divided by median. Two-way analysis of variance (ANOVA) was used to analyze the health effects of indoor air pollution exposure according to BMI. Our study showed that higher levels of SBP, DBP and HR occurred in subjects who were overweight or obese as compared to those with normal weight. Moreover, there was higher level of SBP in subjects who were overweight or obese when they were exposed to higher levels of TVOC and fungi (p<0.05). We also found higher value for DBP and HR with increasing BMI to be associated with exposure to higher TVOC levels. This study suggests that individuals with higher BMI have higher cardiovascular disease risk when they are exposed to poor indoor air quality (IAQ), and specifically in terms of TVOC.
Science of The Total Environment 09/2015; 539:271-276. DOI:10.1016/j.scitotenv.2015.08.158 · 4.10 Impact Factor
"The fact that leptin deficient (ob/ob) and leptin receptor deficient (db/db) mice are hyperresponsive is also supportive of the bronchodilator effect of leptin (Arteaga-Solis et al. 2013; Johnston, et al. 2007; Lu, et al. 2006; Shore, et al. 2003). Leptin and leptin receptor deficiencies also worsen AHR in a murine model of asthma elicited by ozone exposure (Lu et al. 2006; Shore et al. 2003). In addition, infusion of leptin intracerebroventricularly successfully inhibits AHR observed in high fat diet-induced obese mice, ob/ob but not db/db mice, as well as in mice with allergic airway inflammation (Arteaga-Solis et al. 2013). "
[Show abstract][Hide abstract] ABSTRACT: Asthma is a prevalent respiratory disorder triggered by a variety of inhaled environmental factors, such as allergens, viruses and pollutants. Asthma is characterized by an elevated activation of the smooth muscle surrounding the airways, as well as a propensity of the airways to narrow excessively in response to a spasmogen (i.e. contractile agonist), a feature called airway hyperresponsiveness. The level of airway smooth muscle activation is putatively controlled by mediators released in its vicinity. In asthma, many mediators that affect airway smooth muscle contractility originate from inflammatory cells that are mobilized into the airways, such as eosinophils. However, mounting evidence indicates that mediators released by remote organs can also influence the level of activation of airway smooth muscle, as well as its level of responsiveness to spasmogens and relaxant agonists. These remote mediators are transported through circulating blood to act either directly on airway smooth muscle or indirectly via the nervous system by tuning the level of cholinergic activation of airway smooth muscle. Indeed, mediators generated from a diversity of organs, including the adrenals, pancreas, adipose tissues, gonads, heart, intestines and stomach affect the contractility of airway smooth muscle. Together, these results suggest that, apart from a paracrine mode of regulation, airway smooth muscle is subjected to an endocrine mode of regulation. The results also imply that defects in organs other than the lungs can contribute to asthma symptoms and severity. In this review, I suggest that the endocrine mode of regulation of airway smooth muscle contractility is overlooked.
Journal of Endocrinology 06/2014; 222(2). DOI:10.1530/JOE-14-0220 · 3.72 Impact Factor
"However, AHR or eosinophilic inflammation in lung tissue was not augmented by obesity per se. This finding is in contrast with the results of previous studies showing that AHR is a common feature of murine obesity.12,13 In the present study, we used a diet-induced obesity model with C57BL/6J mice. "
[Show abstract][Hide abstract] ABSTRACT: Purpose
Obesity has been suggested to be linked to asthma. However, it is not yet known whether obesity directly leads to airway hyperreactivity (AHR) or obesity-induced airway inflammation associated with asthma. We investigated obesity-related changes in adipokines, AHR, and lung inflammation in a murine model of asthma and obesity.
Materials and Methods
We developed mouse models of chronic asthma via ovalbumin (OVA)-challenge and of obesity by feeding a high-fat diet, and then performed the methacholine bronchial provocation test, and real-time PCR for leptin, leptin receptor, adiponectin, adiponectin receptor (adipor1 and 2), vascular endothelial growth factor (VEGF), transforming growth factor (TGF) β, and tumor necrosis factor (TNF) α in lung tissue. We also measured cell counts in bronchoalveolar lavage fluid.
Both obese and lean mice chronically exposed to OVA developed eosinophilic lung inflammation and AHR to methacholine. However, obese mice without OVA challenge did not develop AHR or eosinophilic inflammation in lung tissue. In obese mice, lung mRNA expressions of leptin, leptin receptor, VEGF, TGF, and TNF were enhanced, and adipor1 and 2 expressions were decreased compared to mice in the control group. On the other hand, there were no differences between obese mice with or without OVA challenge.
Diet-induced mild obesity may not augment AHR or eosinophilic lung inflammation in asthma.
Yonsei medical journal 11/2013; 54(6):1430-7. DOI:10.3349/ymj.2013.54.6.1430 · 1.29 Impact Factor
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