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      The effect of obesity on lung function

      1 , 1
      Expert Review of Respiratory Medicine
      Informa UK Limited

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          Abstract

          <div class="section"> <a class="named-anchor" id="S1"> <!-- named anchor --> </a> <h5 class="section-title" id="d5027508e109">Introduction:</h5> <p id="P1">There is a major epidemic of obesity, and many obese patients suffer with respiratory symptoms and disease. The overall impact of obesity on lung function is multi-factorial, related to mechanical and inflammatory aspects of obesity. </p> </div><div class="section"> <a class="named-anchor" id="S2"> <!-- named anchor --> </a> <h5 class="section-title" id="d5027508e114">Areas Covered:</h5> <p id="P2">Obesity causes substantial changes to the mechanics of the lungs and chest wall, these mechanical changes cause asthma and asthma-like symptoms such as dyspnea, wheeze and airway hyperresponsiveness. Excess adiposity is also associated with increased production of inflammatory cytokines and immune cells that may also lead to disease. This article reviews the literature addressing the relationship between obesity and lung function, and studies addressing how the mechanical and inflammatory effects of obesity might lead to changes in lung mechanics and pulmonary function in obese adults and children. </p> </div><div class="section"> <a class="named-anchor" id="S3"> <!-- named anchor --> </a> <h5 class="section-title" id="d5027508e119">Expert Commentary:</h5> <p id="P3">Obesity has significant effects on respiratory function, which contribute significantly to the burden of respiratory disease. These mechanical effects are not readily quantified with conventional pulmonary function testing and measurement of BMI. Changes in mediators produced by adipose tissue likely also contribute to altered lung function, though as of yet this is poorly understood. </p> </div>

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          Most cited references105

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          Overweight, obesity, and incident asthma: a meta-analysis of prospective epidemiologic studies.

          Although obesity has been implicated as an asthma risk factor, there is heterogeneity in the published literature regarding its role in asthma incidence, particularly in men. To quantify the relationship between categories of body mass index (BMI) and incident asthma in adults and to evaluate the impact of sex on this relationship. Online bibliographic databases were searched for prospective studies evaluating BMI and incident asthma in adults. Independent observers extracted data regarding annualized asthma incidence from studies meeting predetermined criteria, within defined categories of normal weight (BMI or= 30). Data were analyzed by inverse-variance-weighted, random-effects meta-analysis. Stratified analysis between BMI categories and within sex was performed. Seven studies (n=333,102 subjects) met inclusion criteria. Compared with normal weight, overweight and obesity (BMI >or= 25) conferred increased odds of incident asthma, with an odds ratio (OR) of 1.51 (95% confidence interval [CI], 1.27-1.80). A dose-response effect of elevated BMI on asthma incidence was observed; the OR for incident asthma for normal-weight versus overweight subjects was 1.38 (95% CI, 1.17-1.62) and was further elevated for normal weight versus obesity (OR, 1.92; 95% CI, 1.43-2.59; p<0.0001 for the trend). A similar increase in the OR of incident asthma due to overweight and obesity was observed in men (OR, 1.46; 95% CI, 1.05-2.02) and women (OR, 1.68; 95% CI, 1.45-1.94; p=0.232 for the comparison). Overweight and obesity are associated with a dose-dependent increase in the odds of incident asthma in men and women, suggesting asthma incidence could be reduced by interventions targeting overweight and obesity.
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            Universal physical responses to stretch in the living cell.

            With every beat of the heart, inflation of the lung or peristalsis of the gut, cell types of diverse function are subjected to substantial stretch. Stretch is a potent stimulus for growth, differentiation, migration, remodelling and gene expression. Here, we report that in response to transient stretch the cytoskeleton fluidizes in such a way as to define a universal response class. This finding implicates mechanisms mediated not only by specific signalling intermediates, as is usually assumed, but also by non-specific actions of a slowly evolving network of physical forces. These results support the idea that the cell interior is at once a crowded chemical space and a fragile soft material in which the effects of biochemistry, molecular crowding and physical forces are complex and inseparable, yet conspire nonetheless to yield remarkably simple phenomenological laws. These laws seem to be both universal and primitive, and thus comprise a striking intersection between the worlds of cell biology and soft matter physics.
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              Obesity and asthma: an inflammatory disease of adipose tissue not the airway.

              Obesity is a major risk factor for asthma; the reasons for this are poorly understood, although it is thought that inflammatory changes in adipose tissue in obesity could contribute to airway inflammation and airway reactivity in individuals who are obese. To determine if inflammation in adipose tissue in obesity is related to late-onset asthma, and associated with increased markers of airway inflammation and reactivity. We recruited a cohort of obese women with asthma and obese control women. We followed subjects with asthma for 12 months after bariatric surgery. We compared markers in adipose tissue and the airway from subjects with asthma and control subjects, and changes in subjects with asthma over time. Subjects with asthma had increased macrophage infiltration of visceral adipose tissue (P < 0.01), with increased expression of leptin (P < 0.01) and decreased adiponectin (p < 0.001) when controlled for body mass index. Similar trends were observed in subcutaneous adipose tissue. Airway epithelial cells expressed receptors for leptin and adiponectin, and airway reactivity was significantly related to visceral fat leptin expression (rho = -0.8; P < 0.01). Bronchoalveolar lavage cytokines and cytokine production from alveolar macrophages were similar in subjects with asthma and control subjects at baseline, and tended to increase 12 months after surgery. Obesity is associated with increased markers of inflammation in serum and adipose tissue, and yet decreased airway inflammation in obese people with asthma; these patterns reverse with bariatric surgery. Leptin and other adipokines may be important mediators of airway disease in obesity through direct effects on the airway rather than by enhancing airway inflammation.
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                Author and article information

                Journal
                Expert Review of Respiratory Medicine
                Expert Review of Respiratory Medicine
                Informa UK Limited
                1747-6348
                1747-6356
                August 09 2018
                September 02 2018
                August 14 2018
                September 02 2018
                : 12
                : 9
                : 755-767
                Affiliations
                [1 ] Division of Pulmonary and Critical Care Medicine, University of Vermont Larner College of Medicine, Burlington, Vermont, USA
                Article
                10.1080/17476348.2018.1506331
                6311385
                30056777
                67fe4a83-d63a-4f96-8bde-82545a0dface
                © 2018
                History

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