Table of Contents  
ORIGINAL ARTICLE
Year : 2015  |  Volume : 9  |  Issue : 2  |  Page : 118-124

Study of serum leptin level in obese and nonobese asthmatic patients


1 Department of Chest, Faculty of Medicine, Benha University, Benha, Egypt
2 Department of Clinical and Chemical Pathology, Faculty of Medicine, Benha University, Benha, Egypt

Date of Submission27-Mar-2015
Date of Acceptance05-Apr-2015
Date of Web Publication4-Jun-2015

Correspondence Address:
Nabil A Abdelghaffar Hibah
Chest department, Benha University Hospitals, Benha city 13512
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1687-8426.158038

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  Abstract 

Aim: The aim of the study was to investigate serum leptin levels in obese and nonobese asthmatic patients and its change during acute attack and in remission, as well as its relation to the changes in pulmonary functions.
Methods: The study was carried out on 55 participants (40 asthmatic patients and 15 controls) who were divided according to BMI into obese [(BMI >30 kg/m 2 ), 20 asthmatic patients and eight controls] and nonobese [(BMI <25 kg/m 2 ), 20 asthmatic patients and seven controls]. All participants were subjected to calculation of BMI, pulmonary function tests, and morning serum leptin level estimation (after at least 8 h of fasting).
Results: Serum leptin levels (mean in ng/ml) in obese controls (64 ng/ml) and obese asthmatic patients (80.4 ng/ml during remission and 92.9 during exacerbation) were significantly higher than that in nonobese controls (6.3 ng/ml) and nonobese asthmatic patients (33.8 ng/ml during remission and 48.8 during exacerbation). There was a significant (r = −0.456 and P ≤ 0.05) negative correlation between the change in serum leptin (ng/ml) and the change in forced vital capacity (FVC) (% Predicted) and forced expiratory volume in first second (FEV 1 ) (% Predicted) in obese asthmatic patients, but not in nonobese asthmatic patients. There was a significant positive correlation between BMI (kg/m 2 ) and serum leptin levels (ng/ml) in obese (r = 0.712 and P ≤ 0.05) and nonobese (r = 0.747 and P ≤ 0.05) controls and a higher significant positive correlation in obese (r = 0.94 during exacerbation and r = 0.833 during remission, P ≤ 0.001) and nonobese (r = 0.687 during exacerbation, P ≤ 0.001 and r = 0.488 during remission, P ≤ 0.05) asthmatic patients.
Conclusion: Serum leptin levels were higher in all asthmatic patients (more during exacerbation) compared with controls and the values were higher in obese than in nonobese asthmatic patients with a significant negative correlation between the change in serum leptin and the change in FEV 1 and FVC in obese asthmatic patients. These findings indicate that leptin is involved in asthma inflammation.

Keywords: Asthma , BMI , leptin , obese , pulmonary function tests


How to cite this article:
Mohammed EA, Omar MM, Abdelghaffar Hibah NA, Essa HA. Study of serum leptin level in obese and nonobese asthmatic patients. Egypt J Bronchol 2015;9:118-24

How to cite this URL:
Mohammed EA, Omar MM, Abdelghaffar Hibah NA, Essa HA. Study of serum leptin level in obese and nonobese asthmatic patients. Egypt J Bronchol [serial online] 2015 [cited 2020 Mar 31];9:118-24. Available from: http://www.ejbronchology.eg.net/text.asp?2015/9/2/118/158038


  Introduction Top


Asthma is 'a chronic inflammatory disorder of the airways associated with airway hyper-responsiveness that leads to recurrent episodes of widespread, and often reversible, airflow obstruction within the lung' [1].

Obesity has been significantly associated with nonatopic asthma rather than with atopic asthma in women and children [2]. Some studies indicate that obesity may increase asthma severity and may reduce the efficacy of standard asthma medications [3],[4].

Growing evidence suggests that the proinflammatory effects of leptin may contribute to the higher incidence of asthma in the obese population [5],[6].


  Aim of the study Top


The aim was to study serum leptin levels in obese and nonobese asthmatic patients and its change during acute attack and in remission as well as its relation to the changes in pulmonary functions.


  Methods Top


This study was carried out on 55 participants (40 asthmatic patients and 15 controls) who were divided according to BMI into obese [(BMI >30 kg/m 2 ), 20 asthmatic patients and eight controls] and nonobese [(BMI <25 kg/m 2 ), 20 asthmatic patients and seven controls]. Patients with any comorbidity that may affect the serum leptin level [7] (cardiovascular disease, cerebral vascular diseases, diabetes mellitus, liver cirrhosis, end-stage renal disease, tuberculosis, bronchiectasis, malignancy, and connective tissue disorders) and individuals with BMI 25-30 kg/m 2 were excluded from the study.

All participants were subjected to full history taking, thorough clinical examination, plain chest radiography, laboratory investigations (complete blood count, erythrocyte sedimentation rate, liver function tests, kidney function tests, fasting and postprandial blood sugar), and pulmonary function tests (FEV 1 %, FVC%, FEF25-75%, and FEV 1 /FVC were measured for each patient before and 10 min after inhalation of 200-400 mg salbutamol). Body weight (kg) and height (meters) were measured for each patient for calculation of BMI. Serum leptin levels were determined (morning sample after at least 8 h of fasting) during acute exacerbation and after control of the attack and also in the control group by taking blood samples, subjecting them to centrifugation, and then measuring using an ELISA kit (DRG Diagnostics, Marburg, Germany).

Statistical analysis

Results are given as mean ± SD. Differences between groups were statistically analyzed using an unpaired Student t-test. For patients with leptin values below the detection limit (0.25 ng/ml) the value 0.25 ng/ml was used in the analysis. After curve estimation, linear, exponential, or logarithmic Pearson product moment correlation was calculated. After the simple correlations, a regression model was fitted to the data to select the variables that contributed to the explained variation in plasma leptin concentration. Significance was determined at the 5% level. Data were analyzed using statistical package for the social sciences, version 14.0 for Windows (SPSS Inc., Chicago, Illinois, USA).


  Results Top


This study included 38 female (95%) and two male (5%) patients.

[Table 1] shows the age and BMI of obese (mean age ± SD = 34.5 ± 4.44 and mean BMI ± SD = 34.1 ± 1.2) and nonobese (mean age ± SD = 42.4 ± 7.35 and mean BMI ± SD = 23.7 ± 1) controls and obese (mean age ± SD = 42.65 ± 8.98 and mean BMI ± SD = 35.15 ± 3.32) and nonobese (mean age ± SD = 42.5 ± 8.88 and mean BMI ± SD = 23.15 ± 1.81) asthmatic patients.
Table 1: Comparison of age (years) among the studied groups

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[Table 2] shows the statistical comparison of the pulmonary function tests between obese and nonobese controls with nonsignificant differences between all parameters.
Table 2: Statistical comparison of the pulmonary function tests among the studied groups

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[Table 3] shows that serum leptin levels (ng/ml) in obese controls were significantly higher than that in nonobese controls with a mean of 64 ng/ml in obese controls and 6.3 ng/ml in nonobese controls.
Table 3: Comparison of serum leptin (ng/ml) in obese and nonobese controls

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[Table 4] shows that serum leptin (ng/ml) was significantly higher in obese asthmatic patients during an attack than in obese asthmatic patients during remission and in obese controls.
Table 4: Comparison of serum leptin (ng/ml) in obese controls and obese asthmatic patients during attack and remission

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[Table 5] shows that serum leptin (ng/ml) was significantly higher in nonobese asthmatic patients during an attack than in nonobese asthmatic patients during remission and in nonobese controls.
Table 5: Comparison of serum leptin (ng/ml) in nonobese controls and nonobese asthmatic patients during attack and
remission


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[Table 6] shows that serum leptin (ng/ml) was significantly higher in obese than in nonobese asthmatic patients both during an attack and during remission.
Table 6: Comparison of serum leptin (ng/ml) in obese and nonobese asthmatic patients during an attack

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[Table 7] shows that serum leptin (ng/ml) was significantly increased in both obese and nonobese asthmatic patients during an attack than during remission.
Table 7: Comparison of serum leptin (ng/ml) in obese and nonobese asthmatic patients during attack and remission

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[Table 8] shows the nonsignificant negative correlation between serum leptin (ng/ml), FVC (% Predicted), and FEF 25-75 (% Predicted) in obese controls, nonsignificant positive correlation between serum leptin (ng/ml), FEV 1 (% Predicted), and FEV 1 /FVC in obese controls, and nonsignificant positive correlation between serum leptin (ng/ml), FEV 1 (% Predicted), FVC (% Predicted), FEV 1 /FVC, and FEF25-75 (% Predicted) in nonobese controls.
Table 8: Correlations between serum leptin (ng/ml) and pulmonary function tests in obese and nonobese controls

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[Table 9] shows the significant negative correlation between change in serum leptin (ng/ml) and change in FVC (% Predicted) and FEV 1 (% Predicted) in obese asthmatic patients, the nonsignificant positive correlation between change in serum leptin (ng/ml) and change in FEV 1 /FVC and FEF25-75 (% Predicted) in obese asthmatic patients, the nonsignificant negative correlation between the change in serum leptin (ng/ml) and the change in FVC (% Predicted) and FEV 1 (% Predicted) in nonobese asthmatic patients, and the nonsignificant positive correlation between change in serum leptin (ng/ml) and change in FEV 1 /FVC and FEF25-75 (% Predicted) in nonobese asthmatic patients.
Table 9: Correlations between changes in serum leptin (ng/ml) and changes in pulmonary function test scores in obese and nonobese asthmatic patients during attack and remission

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[Table 10] shows that there was a nonsignificant negative correlation between age (years) and serum leptin (ng/ml) in obese and a significant negative correlation between age (years) and serum leptin (ng/ml) in nonobese controls.
Table 10: Correlation between serum leptin and age in obese and nonobese controls

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There was a nonsignificant positive correlation between age (years) and serum leptin (ng/ml) in obese asthmatic patients during an attack and during remission [Table 11]. There was significant positive correlation between age (years) and serum leptin levels (ng/ml) in nonobese asthmatic patients during an attack and during remission.
Table 11: Correlation between serum leptin (ng/ml) and age (years) in obese and nonobese asthmatic patients during attack and remission

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[Table 12] shows the significant positive correlation between BMI (kg/m 2 ) and serum leptin levels (ng/ml) in obese and nonobese controls.
Table 12: Correlation between serum leptin and BMI in obese and nonobese controls

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[Table 13] shows the highly significant positive correlation between BMI (kg/m 2 ) and serum leptin (ng/ml) in obese asthmatic patients during an attack and during remission. There was a highly significant positive correlation between BMI (kg/m 2 ) and serum leptin levels (ng/ml) in nonobese asthmatic patients during an attack and a significant positive correlation during remission.
Table 13: Correlation between serum leptin (ìg/ml) and BMI (kg/m2) in obese and nonobese asthmatic patients during attack and remission

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  Discussion Top


Obesity and bronchial asthma are both chronic, prevalent conditions that pose a significant challenge to the clinician as well as to public health worldwide [8].

The aim of our study was to investigate serum leptin levels in obese and nonobese asthmatic patients and its change during acute attack and during remission as well as its relation to the changes in pulmonary functions.

This study included 38 female (95%) and two male (5%) patients, indicating a higher frequency and morbidity of bronchial asthma in women compared with men. In our study all asthmatic patients were admitted as inpatients in the chest department, Benha University Hospitals. Other studies showed much higher frequency of asthma and associated morbidity in women (regardless of their BMI) compared with men [9],[10],[11],[12].

In our study serum leptin levels in all asthmatic patients were much higher than that in controls and this was statistically significant and increased sharply during acute exacerbation and decreased after control of the attack; however, it was still higher than in the control group, and the level in obese asthmatic patients was higher than the level in nonobese asthmatic patients, which may indicate a role for leptin in asthma pathogenesis.

Our results agreed with data from the Nurses' Health Study [13], which evaluated the relationship between body weight and the incidence of self-reported physician-diagnosed asthma in women. That study included 85 911 patients and was conducted over 4 years. As in the case-control studies, those investigators found a significant relationship between BMI and the incidence of asthma, with obesity increasing the asthma risk by 2.7-3.8-fold and overweight increasing the risk by 50-70%.

Haynes et al. [14] concluded that leptin could predispose to asthma through its effect on immune function [tumor necrosis factor-a (TNF-a) and interleukin-6 (IL-6)] and its effect on the sympathetic nervous system; in addition, Guler et al. [15] found that the median serum leptin concentrations of children (especially boys) were significantly higher in those with asthma than in healthy controls (3.53 vs. 2.26 ng/ml, P = 0.01), even though there was no difference in BMI levels.

Our study also agreed with that by Mai et al. [16] involving children born with very low birth weight who subsequently became overweight. The study showed that current asthmatic patients had median leptin concentrations twice as high as that in children without current asthma (30.8 vs. 14.3 ng/ml, P = 0.14), but this was not the case in nonoverweight children. Taken together, our study and prior studies suggest that leptin may potentially play an important role in the pathophysiology of asthma.

In a study [17] conducted on 5876 individuals after exclusion of those who were either pregnant or had missing values for covariates it was found that adults with the highest quartile of leptin concentrations had an odds ratio (OR) of 1.56 (95% confidence interval 0.96-2.53) for current asthma after adjustment in a multivariable logistic regression analysis for age, sex, race/ethnicity, educational status, smoking status, concentration of cotinine, physical activity, and atopy. This association was stronger in women (OR 1.85) than in men (OR 1.27). In women, adjustment for triceps skin fold thickness strengthened the association between serum leptin concentrations and asthma, whereas adjustment for BMI weakened this association.

Kilic et al. [18] found that the median leptin level was higher in patients with uncontrolled asthma than in those with controlled asthma, but the difference was not significant. In the obese group, a nonsignificant negative correlation (r = -0.138, P = 0.390) was found between leptin levels and asthma control test scores. In the nonobese group, mean unadjusted leptin concentrations were higher in participants who had current asthma than in those who had never had asthma.

Shore et al. [5] found that leptin concentrations are increased acutely during inflammation and, in turn, promote inflammation. Other experiments showed a prompt dose-dependent increase in serum leptin levels and leptin mRNA expression in the adipose tissue of mice following administration of proinflammatory cytokines such as TNF-a and IL-1 [19],[20] as well as demonstration of increased serum TNF-a, IL-6, and IL-12 levels and increased phagocytosis by macrophages on exogenous administration of leptin [21]. Inflammatory mediators such as TNF-a also promote the expression and release of leptin from the adipose tissue, formulating a positive feedback mechanism [22].

Vernooy et al. also reported that leptin had an effect on inflammation through enhancement of production of TNF-a and IL-6 from endotoxin-treated macrophages and lymphocytes [23].

In our study there was a significant negative correlation between serum leptin and both FVC and FEV 1 in obese asthmatic patients but not in nonobese asthmatic patients.

Our findings agreed with a population-based study [24] in which individuals with impaired lung function had raised serum leptin levels; King et al. [25] also reported declines in airway conductance in obese compared with nonobese individuals, which could reflect the proinflammatory role of leptin.

In our study there was a significant positive correlation between BMI (kg/m 2 ) and serum leptin levels (ng/ml) in obese and nonobese control and asthmatic individuals.

Several studies have identified an association between asthma and obesity in women [9],[13],[18]. BMI was positively associated with asthma, wheezing, asthma treatment, atopy, and immunoglobulin E, and inversely with the FEV 1 /FVC ratio in women. One would expect that most obese individuals would become short of breath much more quickly, especially if some of them had exercise-induced asthma. It remains unclear whether this association is due to asthma itself or due to symptoms caused by overweight or adipokines such as leptin.

Hancox et al. [26] reported that a raised BMI was associated with asthma and atopy in women than in men, and population attributable fraction calculations estimated that 28% (95% confidence interval 7-45) of asthma cases in women after age 9 are due to overweight.

Guler et al. [15] noted that, even after controlling the BMI, serum leptin is higher in male asthmatic patients compared with nonasthmatic individuals.

Some studies have suggested that leptin may play an important role in asthma pathophysiology through its ability to activate the sympathetic nerves. Leptin was found to increase the activity of sympathetic nerves in various organs, but its effects on the lung sympathetic nerves are unknown [14],[27],[28]. In animal studies, leptin-treated mice were found to exhibit augmented responses to metacholine and increased levels of IgE, following ovalbumin challenge, when compared with saline-infused mice.

Leptin release from adipose tissue or the lung may be induced by disease-related inflammation, which further increases the airway inflammation and hyper-reactivity [17, 29, 30]. Leptin has been identified to have proinflammatory properties through the stimulation of TNF-a and IL-6 from the adipose tissue [31], and through the modulation of immunity to promote Th1 immune responses with increased production of interferon-c (IFN-g) [32]. In asthmatic children, IFN-g-producing CD4+ T cells are inversely correlated with blood eosinophilia but positively correlated with airway hyper-responsiveness, suggesting a possible involvement of IFN-g in nonatopic asthma [33].

In our study there was a significant negative correlation between change in serum leptin (ng/ml) and change in both FVC (% Predicted) and FEV 1 (% Predicted) in obese asthmatic patients but not in nonobese asthmatic patients. This finding may indicate that leptin has an effect on airway response in obese asthmatic patients during exacerbation.


  Conclusion Top


Serum leptin levels were higher in all asthmatic patients (more during exacerbation) than in controls and the values were higher in obese than in nonobese asthmatic patients with a significant negative correlation between the change in serum leptin and the change in FEV 1 and FVC in obese asthmatic patients. These findings indicate that leptin is involved in asthma inflammation.


  Acknowledgements Top


Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Bateman ED, Hurd SS, Barnes PJ, Bousquet J, Drazen JM, FitzGerald M, et al. Global strategy for asthma management and prevention: GINA executive summary. Eur Respir J 2008; 31 :143-178.  Back to cited text no. 1
    
2.
Chen Y, Dales R, Jiang Y. The association between obesity and asthma is stronger in nonallergic than allergic adults. Chest 2006; 130 :890-895.  Back to cited text no. 2
    
3.
Peters-Golden M, Swern A, Bird SS, Hustad CM, Grant E, Edelman JM. Influence of body mass index on the response to asthma controller agents. Eur Respir J 2006; 27 :495-503.  Back to cited text no. 3
    
4.
Figueroa-Munoz JI, Chinn S, Rona RJ. Association between obesity and asthma in 4-11 year old children in the UK. Thorax 2001; 56 :133-137.  Back to cited text no. 4
    
5.
Shore SA, Rivera-Sanchez YM, Schwartzman IN, Johnston RA. Responses to ozone are increased in obese mice. J Appl Physiol 2003; 95 :938-945.  Back to cited text no. 5
    
6.
Shore SA, Schwartzman IN, Mellema MS, Flynt L, Imrich A, Johnston RA. Effect of leptin on allergic airway responses in mice. J Allergy Clin Immunol 2005; 115 :103-109.  Back to cited text no. 6
    
7.
F Lago, C Dieguez, J Gómez-Reino, O Gualillo. Adipokines as emerging mediators of immune response and inflammation. Nat Clin Pract Rheumatol 2007; 3 :716-724.  Back to cited text no. 7
    
8.
DA Beuther. Obesity and asthma. Clin Chest Med 2009; 30 :479-488.  Back to cited text no. 8
    
9.
Chen Y, Dales R, Tang M, Krewski D. Obesity may increase the incidence of asthma in women but not in men: longitudinal observations from the Canadian National Population Health Surveys. Am J Epidemiol 2002; 155 :191-197.  Back to cited text no. 9
    
10.
Leynaert B, Bousquet J, Henry C, Liard R, Neukirch F. Is bronchial hyperresponsiveness more frequent in women than in men? A population-based study. Am J Respir Crit Care Med 1997; 156 :1413-1420.  Back to cited text no. 10
    
11.
Torén K, Hermansson BA. Incidence rate of adult-onset asthma in relation to age, sex, atopy and smoking: a Swedish population-based study of 15813 adults. Int J Tuberc Lung Dis 1999; 3 :192-197.  Back to cited text no. 11
    
12.
K Tantisira, S Weiss. Complex interactions in complex traits: obesity and asthma. Thorax 2001; 56 :ii64-ii73.  Back to cited text no. 12
    
13.
Camargo CA Jr, Weiss ST, Zhang S, Willett WC, Speizer FE. Prospective study of body mass index, weight change, and risk of adult-onset asthma in women. Arch Intern Med 1999; 159 :2582-2588.  Back to cited text no. 13
    
14.
Haynes WG, Morgan DA, Djalali A, Sivitz WI, Mark AL. Interactions between the melanocortin system and leptin in control of sympathetic nerve traffic. Hypertension 1999; 33 :542-547.  Back to cited text no. 14
    
15.
Guler N, Kirerleri E, Ones U, Tamay Z, Salmayenli N, Darendeliler F. Leptin: does it have any role in childhood asthma? J Allergy Clin Immunol 2004; 114 :254-259.  Back to cited text no. 15
    
16.
Mai XM, Böttcher MF, Leijon I. Leptin and asthma in overweight children at 12 years of age. Pediatr Allergy Immunol 2004; 15 :523-530.  Back to cited text no. 16
    
17.
Sood A, Ford ES, Camargo CA Jr. Association between leptin and asthma in adult. Thorax 2006; 61 :300-305.  Back to cited text no. 17
    
18.
Kilic H, Oguzulgen IK, Bakir F, Turktas H. Asthma in obese women: outcomes and factors involved. J Investig Allergol Clin Immunol 2011; 21 :290-296.  Back to cited text no. 18
    
19.
Sarraf P, Frederich RC, Turner EM, Ma G, Jaskowiak NT, Rivet DJ 3rd, et al. Multiple cytokines and acute inflammation raise mouse leptin levels: potential role in inflammatory anorexia. J Exp Med 1997; 185 :171-175.  Back to cited text no. 19
    
20.
Faggioni R, Fantuzzi G, Fuller J, et al. IL-1 beta mediates leptin induction during inflammation. Am J Physiol 1998; 274 :R204-R208.  Back to cited text no. 20
    
21.
Gosset P, Tsicopoulos A, Wallaert B, Joseph M, Capron A, Tonnel AB. Tumor necrosis factor alpha and interleukin-6 production by human mononuclear phagocytes from allergic asthmatics after IgE-dependent stimulation. Am Rev Respir Dis 1992; 146 :768-774.  Back to cited text no. 21
    
22.
Kirchgessner TG, Uysal KT, Wiesbrock SM, Marino MW, Hotamisligil GS. Tumor necrosis factor-alpha contributes to obesity-related hyperleptinemia by regulating leptin release from adipocytes J Clin Invest 1997; 100 :2777-2782.  Back to cited text no. 22
    
23.
JHJ Vernooy, NDJ Ubag, GG Brusselle, J Tavernier, BT Suratt, GF Joos, et al. Leptin as regulator of pulmonary immune responses: involvement in respiratory diseases. Pulm Pharmacol Ther 2013; 26 :464-472.  Back to cited text no. 23
    
24.
Sin DD, Man SF. Impaired lung function and serum leptin in men and women with normal body weight: a population based study. Thorax 2003; 58 :695-698.  Back to cited text no. 24
    
25.
King GG, Brown NJ, Diba C, Thorpe CW, Muñoz P, Marks GB, et al. The effects of body weight on airway calibre. Eur Respir J 2005; 25 :896-901.  Back to cited text no. 25
    
26.
Hancox RJ, Milne BJ, Poulton R, Taylor DR, Greene JM, McLachlan CR, et al. Sex differences in the relation between body mass index and asthma and atopy in a birth cohort. Am J Respir Crit Care Med 2005; 171 :440-445.  Back to cited text no. 26
    
27.
Weiss ST. Obesity: insight into the origins of asthma. Nat Immunol 2005; 6 :537-539.  Back to cited text no. 27
    
28.
Weiss ST, Shore S. Obesity and asthma: directions for research. Am J Respir Crit Care Med 2004; 169 :963-968.  Back to cited text no. 28
    
29.
Shore SA. Obesity and asthma: lessons from animal models. J Appl Physiol 2007; 102 :516-528.  Back to cited text no. 29
    
30.
Shore SA. Obesity and asthma: possible mechanisms. J Allergy Clin Immunol 2008; 121 :1087-1093. quiz 1094-1085  Back to cited text no. 30
    
31.
Bastard JP, Maachi M, Lagathu C, Kim MJ, Caron M, Vidal H, et al. Recent advances in the relationship between obesity, inflammation, and insulin resistance. Eur Cytokine Netw 2006; 17 :4-12.  Back to cited text no. 31
    
32.
Matarese G, La Cava A, Sanna V, Lord GM, Lechler RI, Fontana S, et al. Balancing susceptibility to infection and autoimmunity: a role for leptin? Trends Immunol 2002; 23 :182-187.  Back to cited text no. 32
    
33.
Kim JH, Kim BS, Lee SY, Seo JH, Shim JY, Hong TJ, et al. Different IL-5 and IFN-gamma production from peripheral blood T-cell subsets in atopic and nonatopic asthmatic children. J Asthma 2004; 41 :869-876.  Back to cited text no. 33
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11], [Table 12], [Table 13]


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