The relationship between adiponectin levels and epicardial adipose tissue thickness in non-obese children with asthma
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Updated: Mar 28, 2026

Assessment of Child Anthropometry in a Large Epidemiologic Study
Published on: February 2, 2017
Cem Ozde1, Mahmut Dogru, Firat Erdogan
1Department of Cardiology, Gaziosmanpasa Taksim Education and Research Hospital, Istanbul, Turkey.
Insights
Epicardial adipose tissue thickness (EATT) is higher in children with asthma. Lower serum adiponectin (APN) levels in these children may indicate a pro-inflammatory state, suggesting a link between EATT and asthma severity.
Area of Science:
- Pediatric Allergy and Immunology
- Cardiology
- Endocrinology
Background:
- Asthma is associated with adiponectin (APN), but mechanisms are unclear.
- APN, an anti-inflammatory protein, may be secreted by Epicardial Adipose Tissue (EAT).
- This study hypothesizes serum APN levels correlate with EAT accumulation (thickness) in asthmatic children.
Purpose of the Study:
- To investigate serum APN and epicardial adipose tissue thickness (EATT) in non-obese children with asthma versus healthy controls.
- To analyze the relationships between APN, EATT, and clinical outcomes in pediatric asthma.
Main Methods:
- Cross-sectional, observational study of 68 children with asthma and 39 healthy controls.
- EATT measured via transthoracic echocardiography.
- Serum APN levels assessed; statistical analyses included independent t-tests and Spearman correlations.
Main Results:
- Asthma group had significantly higher EATT (p < 0.001) compared to controls.
- Asthma group showed significantly lower serum APN levels (p < 0.001) than controls.
- APN was negatively correlated with EATT (r = -0.266, p = 0.006) in both groups.
Conclusions:
- EATT is associated with non-obese pediatric asthma.
- Elevated EATT may correlate with increased pro-inflammatory cytokines and decreased APN release.
- Low APN levels and high EATT may indicate a pro-inflammatory profile in non-obese asthmatic children.
Background:
There is an association between adiponectin (APN) and asthma. However, the mechanisms underlying this association is unclear. APN is a predominantly anti-inflammatory protein with possible signalling activity in the lung that can be secreted by Epicardial Adipose Tissue (EAT). Our hypothesis is that serum APN levels may be directly and simply related to the amount of EAT accumulation, particularly when it is expressed as thickness in children with asthma.
Objective:
The aim of this study was to investigate whether serum adiponectin (APN) and epicardial adipose tissue thickness (EATT) have an effect in non-obese children with asthma and in healthy non-asthmatic children, and analyze their relationships with clinical outcomes.
Methods:
68 children diagnosed with asthma (20 girls/48 boys) who had applied at the pediatric allergy and clinical immunology clinic of the hospital were included in this cross-sectional, observational study. The age-matched control group included 39 healthy children (18 girls/21 boys). EATT was measured by transthoracic echocardiography. The serum APN levels were also checked. Statistical analysis was performed by using independent sample t-test and Spearman correlation analyses.
Results:
The mean age of the asthma group was 10.2 ± 2.7 years, and the average EATT was found to be 5.1 ± 0.1 mm. The mean age of the control group was 10.5 ± 2.8 years, and the average EATT was found to be 5.1 ± 0.7 mm. The EATT of the asthma group was found to be significantly higher (p < 0.001) in study group. In the asthma group the APN was 10.0 ± 5.3 mg/L, and in the control group the APN was 15.8 ± 10.5 mg/L (p < 0.001). We found that APN was significantly negatively correlated with EATT (r = -0.266, p = 0.006) in asthma and control groups.
Conclusion:
EATT is associated with non-obese asthmatic children. High EATT may be related with high release of pro-inflammatory cytokine and low release of APN. Low levels of APN may be related to low anti-inflammatory effects. Therefore, high EATT and low levels of APN may indicate pro-inflammantory profiles in non-obese asthmatic children.
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Critical processes in asthma pathophysiology include:
