Impaired glucose metabolism and bronchial hyperresponsiveness in obese prepubertal asthmatic children
Nikolaos Karampatakis1, Theodoros Karampatakis2, Assimina Galli-Tsinopoulou1
14th Department of Pediatrics, Medical School, Papageorgiou General Hospital of Thessaloniki, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Insights
Obesity does not directly cause airway hyperreactivity in children with asthma. Instead, the combination of obesity with insulin resistance and impaired glucose metabolism significantly increases bronchial hyperresponsiveness in asthmatic children.
Area of Science:
- Pediatric Pulmonology
- Metabolic Disorders
- Allergy and Immunology
Background:
- Rising parallel prevalence of asthma and obesity in children.
- Unclear mechanisms linking asthma, obesity, and metabolic dysfunction.
- Need to investigate bronchial hyperresponsiveness (BHR) in relation to obesity and glucose metabolism in children.
Purpose of the Study:
- To investigate the associations between BHR, impaired glucose metabolism, obesity, and asthma in prepubertal children.
- To determine if obesity alone or in conjunction with metabolic issues influences airway hyperresponsiveness.
Main Methods:
- Study included 71 prepubertal children categorized into four groups: healthy controls, non-obese asthmatics, obese non-asthmatics, and obese asthmatics.
- All children underwent spirometry and bronchial hyperresponsiveness testing using mannitol (PD15).
- Insulin resistance was assessed via HOMA-IR, and obese children underwent oral glucose tolerance testing (OGTT).
Main Results:
- Obese asthmatic children exhibited significantly lower PD15 values compared to normal-weight asthmatics.
- Obese asthmatic children with insulin resistance (HOMA-IR ≥2.5) or impaired OGTT showed significantly lower PD15 values.
- Lower PD15 values indicate increased bronchial hyperreactivity.
Conclusions:
- Obesity itself is not directly correlated with airway hyperreactivity in asthmatic children.
- The presence of glucose intolerance and insulin resistance alongside obesity is critical for increased bronchial hyperresponsiveness.
- These findings highlight the complex interplay between metabolic health and respiratory conditions in pediatric asthma.
Introduction:
The prevalence of asthma and obesity has risen in parallel over the last decades, but the exact mechanisms linking these two diseases still remain unclear. The aim of the present study was to investigate the associations between bronchial hyperresponsiveness (BHR), impaired glucose metabolism, obesity, and asthma in prepubertal children.
Methods:
A total of 71 prepubertal children were included in the study and divided in four groups according to the presence of asthma and their Body Mass Index (BMI): Group 1-Healthy Controls (HC), Group 2-Non Obese Asthmatics (NOA), Group 3-Obese Non Asthmatics (ONA), Group 4-Obese Asthmatics (OA) Αll children underwent spirometry and bronchial hyperresponsiveness testing by using the cumulative Provoking Dose of mannitol (PD15, primary study variable); homeostasis model assessment-estimated insulin resistance (HOMA-IR) index was calculated in order to evaluate insulin resistance. Obese children also underwent an oral glucose tolerance testing (OGTT).
Results:
A statistically significant difference in bronchial hyperreactivity (mean ± SD) was detected in the group of obese asthmatic children who had lower values of PD15 , (174.16 ± 126.42) as compared to normal weight asthmatic children (453.93 ± 110.27), (P < 0.001). Moreover, obese asthmatic children with confirmed insulin resistance (HOMA-IR ≥2.5), had significantly lower PD15 values (89.05 ± 42.75) as compared to those with HOMA-IR <2.5 (259.27 ± 125.75), (P = 0.006). Finally, obese asthmatic children with impaired OGTT had likewise significantly lower PD15 (81.02 ± 42.16) measurements as compared to children with normal OGTT (267.3 ± 112.62), (P = 0.001).
Conclusion:
Our findings suggest that obesity per se does not correlate to airway hyperreactivity unless it is accompanied by glucose intolerance and insulin resistance. Pediatr Pulmonol. 2017;52:160-166. © 2016 Wiley Periodicals, Inc.
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