Relationship between Sleep Apnea, Fat Distribution, and Insulin Resistance in Obese Children

Abstract

Background:Obstructive sleep apnea (OSA) is associated with obesity, inflammation, and insulin resistance. The role of fat distribution in OSA pathogenesis has not been established in children. The objective of the study is to examine the relationship between fat distribution, OSA, and insulin resistance in an unselected population of obese children. Methods: All obese (BMI > 95th percentile) children (ages 5-18 y) seen at a pediatric obesity clinic were invited to participate. Subjects underwent polysomnography, and were tested for dyslipidemia, inflammation, and insulin resistance measured by the homeostasis model assessment (HOMA). In a subset of subjects, magnetic resonance (MRI) imaging was used to determine the abdominal visceral and subcutaneous adipose tissue areas and magnetic resonance spectroscopy (MRS) spectroscopy was used to intramyocellular lipids in leg muscles. Measurements and Main Results: 31 obese subjects enrolled and completed polysomnography and serum testing, and 19 subjects underwent MRI/MRS. The mean age was 12.6 ± 3.0 y and the mean body mass index (BMI) was 39.5 ± 11.2 kg/m 2 . Forty-eight percent had OSA (mean apnea hypopnea index [AHI] 6.26 ± 6.77 events/h) Subjects with OSA had significantly increased BMI, log HOMA, triglycerides, and leptin compared to those without OSA. In regression analysis, only BMI z-score was associated with log HOMA. In the subset of patients with imaging data, visceral fat area was strongly predictive of AHI (p = 0.003, r 2 = 0.556). BMI z-score, gender, and age were not predictive. Conclusions: Visceral fat distribution is independently predictive of OSA severity in obese children.

Obstructive sleep apnea in children: a critical update

“…In a community-based study of predominantly postpubertal adolescents, strong associations were demonstrated between OSA and the metabolic syndrome, as well as with individual metabolic parameters, such as fasting insulin and homeostatic model assessment (HOMA) 29,84,85. Sleep fragmentation and intermittent hypoxia were also found to be associated with decreased insulin sensitivity in obese adolescent boys 86.…”

“…Fatty infiltrates within the compartments of the upper airway structures and the neck are likely to result in upper airway narrowing and increased pharyngeal collapsibility. Central obesity also reduces the functional residual capacity of the lungs, due to abdominal visceral fat impinging on the chest cavity limiting diaphragmatic descent, particularly when lying in the supine position;29 in addition, thoracic fat weighing on the chest wall can effectively decrease lung compliance, leading to hypoventilation, atelectasis, and ventilation–perfusion mismatch. The reduced lung volumes may decrease airway stiffness by reducing the tracheal tethering effect, further increasing the risk of upper airway collapse during sleep.…”

Sleep, sleep-disordered breathing and lipid homeostasis: translational evidence from murine models and children

“…Evidence has suggested that, at any level of OSAS severity, the degree of adenotonsillar hypertrophy required to develop OSAS of such magnitude is reduced in obese children [50]. Recent evidence in children has also suggested that OSAS is related to specific areas of fat deposition; more specifically, OSAS severity was shown to be strongly predicted by visceral fat deposition as defined by MRI [51]. Finally, the phenotype of obesity-induced childhood OSAS is markedly different from the OSAS phenotype that is exclusively induced by adenotonsillar hypertrophy [52].…”

Current child, but not maternal, snoring is bi-directionally related to adiposity and cardiometabolic risk markers: A cross-sectional and a prospective cohort analysis

“…A few prospective studies have looked at only inflammation and overweight/obesity in association with snoring and OSA, but not in-depth the complete spectrum of cardiometabolic biomarkers [20,21]. For instance, OSA in obese children was associated with greater visceral fat area derived using MRI [22]. The same investigators also demonstrated that obese children with OSA (versus obese children without OSA) had higher insulin resistance, triglycerides, and leptin [22], whereas another study showed no changes in leptin among children with versus without OSA [23].…”

“…For instance, OSA in obese children was associated with greater visceral fat area derived using MRI [22]. The same investigators also demonstrated that obese children with OSA (versus obese children without OSA) had higher insulin resistance, triglycerides, and leptin [22], whereas another study showed no changes in leptin among children with versus without OSA [23]. …”