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Published on: June 13, 2025
Increased systemic inflammation overnight correlates with insulin resistance among children evaluated for obstructive
Mark D Deboer1, James P Mendoza, Lei Liu
1Division of Pediatric Endocrinology, P.O. Box 800386, Charlottesville, VA 22908, USA. deboer@virginia.edu
Insights
In children suspected of obstructive sleep apnea (OSA), insulin resistance, not OSA severity, may drive overnight inflammation. Further research is needed to understand these links.
Area of Science:
- Pediatric Sleep Medicine
- Endocrinology
- Inflammation Research
Background:
- Obstructive sleep apnea (OSA) in children is linked to obesity, insulin resistance, and elevated inflammation (hsCRP).
- The relationship between OSA, obesity, insulin resistance, and overnight inflammation in children requires further investigation.
Purpose of the Study:
- To determine if inflammation increases overnight in children with suspected OSA.
- To assess if increased inflammation correlates with OSA severity, obesity, or insulin resistance.
Main Methods:
- Twenty-three children underwent sleep studies with hsCRP measured pre- and post-sleep.
- Insulin resistance was calculated using HOMA-IR from fasting glucose and insulin levels.
- Correlations analyzed hsCRP changes (ΔhsCRP) against HOMA-IR, BMI z-score, and sleep study parameters (AHI, O2 saturation).
Main Results:
- hsCRP levels correlated with HOMA-IR and BMI z-scores in the overall cohort.
- Overnight hsCRP change (ΔhsCRP) correlated with HOMA-IR but not BMI z-score.
- Sleep study parameters (AHI, O2 saturation nadirs) did not correlate with hsCRP or ΔhsCRP.
Conclusions:
- Insulin resistance may be a key factor in overnight inflammation increase among children evaluated for OSA.
- Overnight inflammation increase was not linked to OSA severity markers from sleep studies.
- The precise role of OSA in overnight inflammation and its mechanisms remain unclear, necessitating further research.
Purpose:
Obstructive sleep apnea (OSA) in children is associated with obesity, insulin resistance, and elevated baseline inflammation as measured by high-sensitivity C-reactive protein (hsCRP). Our goal was to evaluate whether inflammation increases overnight among children suspected of having OSA and to determine whether worsened inflammation is associated with the degree of OSA severity, obesity, and/or insulin resistance.
Methods:
Twenty-three children with clinical suspicion of OSA underwent a sleep study. Levels of hsCRP were tested the evening before and morning after the sleep study. Fasting insulin and glucose levels were measured from which the homeostasis model of insulin resistance (HOMA-IR) was calculated. Linear correlations were performed to evaluate relationships between hsCRP levels at baseline and change overnight (ΔhsCRP) vs. HOMA-IR, body mass index (BMI) z-score, and sleep study parameters related to O(2) saturation and the apnea-hypopnea index (AHI).
Results:
Among children with OSA and the entire cohort, hsCRP values were correlated with HOMA-IR and BMI z-scores. HOMA-IR but not BMI z-score correlated with ΔhsCRP overnight in the entire cohort. Sleep study parameters, including AHI mean O(2) saturation overnight, REM O(2) nadir, and non-REM O(2) nadir were not correlated with hsCRP or ΔhsCRP overnight.
Conclusion:
Among children being evaluated for OSA, degree of insulin resistance may be an important determinant of increased systemic inflammation overnight. Sleep study markers did not correlate with ΔhsCRP, leaving uncertain the role of OSA in increasing inflammation overnight. Further studies are needed to explore these associations and their potential mechanisms.
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