Obesity and asthma: possible mechanisms. J Allergy Clin Immunol
Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA. The Journal of allergy and clinical immunology
(Impact Factor: 11.48).
06/2008; 121(5):1087-93; quiz 1094-5. DOI: 10.1016/j.jaci.2008.03.004
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.
Available from: Woo-Jung Song
- "Many clinical studies showed the consistent association of obesity with asthma in terms of causal relationship, dose-dependency, and reversal of asthma by intervention, although the precise mechanism between obesity and asthma remains unclear [2, 3, 4, 5, 6]. Several mechanisms have been suggested as possible explanations about the relationship between obesity and asthma, including mechanical effects of obesity on the lung, chronic inflammation, common genetic factors, and comorbid conditions related to obesity such as gastroesophageal ref lux disease and sleep apnea . Obesity is a state of chronic systemic inflammation, and may cause the metabolic complications such as insulin resistance, diabetes mellitus, and cardiovascular disease . "
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ABSTRACT: Several epidemiologic studies showed the significant association of insulin resistance with asthma.
The aim of this study was to evaluate the association of insulin resistance with airway hyperresponsiveness (AHR) in adult population.
1,058 subjects who visited to the Seoul National University Hospital Gangnam Center from October 2007 to January 2009 for a routine health check-up were enrolled. All subjects completed a questionnaire, anthropometric measurements such as body mass index (BMI) and waist circumference, blood tests, pulmonary function test, and methacholine bronchial provocation test (MBPT). Insulin resistance was estimated from the homeostasis model of assessment of insulin resistance (HOMA-IR).
Thirty-three subjects (3.1%) had AHR based on MBPT. The subjects with AHR had higher BMI, waist circumference, and HOMA-IR than those without AHR (p < 0.001, p = 0.003, and p = 0.002, respectively). In case of men, fasting insulin level and HOMA-IR had significant correlation with forced expiratory volume in 1 second (%) (r = -0.1440, p = 0.011, and r = -0.1156, p = 0.042, respectively). Fasting insulin level and HOMA-IR were higher in men with AHR than in those without (p = 0.046 and p = 0.040, respectively). In binary logistic regression analysis after adjustment for age, HOMA-IR was the significant risk factor for AHR in men (HOMA-IR: odds ratio [OR], 3.21; 95% confidence interval [CI], 1.00-10.30). In case of women, fasting insulin, glucose level, or insulin resistance had no significant correlation with lung function. BMI, waist circumference, and HOMA-IR were significantly higher in women with AHR than in those without (p = 0.001, p = 0.011, and p = 0.010, respectively). In binary logistic regression analysis after adjustment for age, BMI and HOMA-IR were the significant risk factors for AHR in women (BMI: OR, 2.20; 95% CI, 1.23-3.82; insulin resistance: OR, 1.05; 95% CI, 1.00-1.09).
Insulin resistance was significantly associated with bronchial hyperreactivity, which is the most characteristic feature of asthma.
04/2014; 4(2):99-105. DOI:10.5415/apallergy.2014.4.2.99
Available from: Farzad Shidfar
- "Obesity is generally considered as a chronic low-grade systemic inflammation. In this regard, recent research has revealed a multitude of changes in gene expression of cytokines , chemokines, acute phase proteins, and other factors of the immune system in obese individuals . Furthermore, the immunological imbalance induced by obesity might also be responsible for the development of inflammatory complications. "
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ABSTRACT: Probiotics are believed to have interaction with immune cells through sustained effects on gene expression of different cytokines and transcription factors. The present randomized doubled-blind controlled clinical trial was performed recruiting 75 individuals with BMI 25-35, who were randomly assigned to the following three groups: Group 1 (n = 25) who consumed regular yogurt as part of a low calorie diet [RLCD], group 2 (n = 25) who received probiotic yogurt with a LCD [PLCD] and group 3 (n = 25) who consumed probiotic yogurt without LCD [PWLCD] for 8 week. Participants in PLCD and PWLCD groups received 200 g/day yogurt containing Lactobacillus acidophilus La5, Bifidobacterium Bb12, and lactobacillus casei DN001 10(8) cfu/gr. The expression of the FOXP3, T-bet, GATA3, TNF-α, IFN-γ, TGF-β, and ROR-γt in PBMCs genes were assessed, before and after intervention. In three groups, ROR-γt expression was reduced (P = 0.007) and FOXP3 was increased (P < 0.001). The expression of TNFα, TGFβ, and GATA3 genes did not change among all groups after intervention. Interestingly, the expression of T-bet gene, which was significantly decreased in PLCD and PWLCD groups (P < 0.001), whereas gene expression of IFN-γ decreased in all three groups. Our results suggest that weight loss diet and probiotic yogurt had synergistic effects on T-cell subset specific gene expression in peripheral blood mononuclear cells among overweight and obese individuals. © 2013 BioFactors, 2013.
BioFactors 11/2013; 39(6). DOI:10.1002/biof.1128 · 4.59 Impact Factor
Available from: PubMed Central
- "However, the mechanism underlying the associations between obesity and asthma has not yet been established. Dietary factors, systemic inflammation, changes in immune function, reduced chest wall compliance, insulin resistance, comorbidities, and common genetic predisposition have been suggested as potential links between the two conditions.5-7 "
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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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