Sleep-Disordered Breathing and the Metabolic Syndrome in Overweight and Obese Children and Adolescents

Verhulst, Stijn; Schrauwen, Nancy; Haentjens, Dominique; Rooman, Raoul; Gaal, Luc Van; Backer, Wilfried A. De; Desager, K N

doi:10.1016/j.jpeds.2007.01.051

Cited by 132 publications

(90 citation statements)

References 37 publications

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“…22 A study by Verhulst and colleagues found that OSA was associated with several elements of the metabolic syndrome, but this was independent of waist circumference. 14 Another study by the same authors demonstrated that several measures of abdominal adiposity (waist circumference, waistto-hip ratio, and percent fat mass measured by bioelectric impedance) correlated with oxygen desaturations associated with brief respiratory pauses, but not OSA. 13 By contrast, our study,…”

Section: Resultsmentioning

confidence: 96%

“…Multiple studies have demonstrated a clear relationship between OSA, insulin resistance, and inflammation in obese and non-obese children. [10][11][12][13][14] Intermittent hypoxemia predisposes to insulin resistance in ani-BRIEF SUMMARY Current Knowledge/Study Rationale: Obesity is a significant risk factor for obstructive sleep apnea in children but not all obese children suffer from OSA. Studies of fat distribution in adults have shown visceral adiposity to be strongly associated with OSA.…”

Section: S C I E N T I F I C I N V E S T I G a T I O N Smentioning

confidence: 99%

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

Canapari

Hoppin

Kinane

et al. 2011

Journal of Clinical Sleep Medicine

103

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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.

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Section: Resultsmentioning

confidence: 96%

Section: S C I E N T I F I C I N V E S T I G a T I O N Smentioning

confidence: 99%

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

Canapari

Hoppin

Kinane

et al. 2011

Journal of Clinical Sleep Medicine

103

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“…Whereas the estimated prevalence of SDB in the general pediatric population is about 2%, studies have shown a much higher prevalence of 13-59% in obese children and adolescents, according to the population studied (1,2). Furthermore, SDB has proven to be an independent risk factor for acquiring different components of the metabolic syndrome in obese patients and the degree of SDB is associated with the severity of some metabolic alterations (3,4).…”

Section: Introductionmentioning

confidence: 99%

Weight Loss and Sleep‐Disordered Breathing in Childhood Obesity: Effects on Inflammation and Uric Acid

Hoorenbeeck

Franckx²,

Debode³

et al. 2012

Obesity

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Sleep‐disordered breathing (SDB) is prevalent in childhood obesity. It may be an independent risk factor for the metabolic syndrome. Possible mechanisms are inflammation and oxidative stress. Adenotonsillectomy in childhood obesity is associated with a high recurrence rate and risk of postoperative weight gain. Therefore, this study assessed the effects of SDB on inflammation and oxidative stress in childhood obesity before and after weight loss. We included 132 obese subjects between 10 and 18 years consecutively. Median age was 15.4 years (10.1–18.0). Mean BMI z‐score was 2.72 ± 0.42. Leukocytes and differentiation, high sensitivity C‐reactive protein (hs‐CRP), and uric acid (UA) were determined at baseline and subjects underwent a sleep assessment. SDB was diagnosed in 39%. Linear regression analysis showed an association between UAlog and oxygen desaturation indexlog (ODIlog) (r = 0.20; P = 0.03), between leukocyteslog and respiratory disturbance indexlog (RDIlog) (r = 0.23; P = 0.01), and between lymphocyteslog and RDIlog (r = 0.19; P = 0.04). Follow‐up was organized after 4–6 months of treatment. Median decrease in BMI z‐score was 32%. Laboratory measurements were repeated. Subjects with SDB at baseline underwent a second sleep study. Of these 49 subjects, 12 showed residual SDB. This corresponds with a treatment success rate of 71%. Unlike changes in inflammatory markers, improvements in UA were associated with improvements in RDI and ODI (respectively: r = 0.44; P = 0.007, r = 0.41; P = 0.01). In conclusion, weight loss is effective in treating obese children with SDB. At baseline, a link exists between inflammation and SDB. Oxidative stress is reflected by UA at baseline and the concentration decreases after treatment according to improvements in SDB.

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“…27 Regardless of symptoms suggesting the presence of sleep apnea, all children were referred because of being overweight. The metabolic syndrome was defined based on the definition proposed by Cook et al 2 ; that is, if three or more of the following were present, the patient was diagnosed with metabolic syndrome: (1) waist circumference X90th percentile adjusted for age and sex; (2) fasting glucose X110 mg per 100 ml; (3) fasting triglycerides X110 mg per 100 ml; (4) fasting high-density lipoproteins cholesterol p40 mg per 100 ml; (5) blood pressure X90th percentile adjusted for age and sex.…”

Section: Sleep-disordered Breathing and The Metabolic Syndromementioning

confidence: 99%

“…36 Insulin resistance is reflected by increased HOMA levels. Two other studies assessed insulin resistance using oral glucose tolerance tests, 27,28 which can be considered an alternative method for studying glucose homeostasis. Unfortunately, no studies have used the insulin clamp technique, which is considered the gold standard for assessing insulin sensitivity.…”

Section: Sleep-disordered Breathing and Insulin Resistancementioning

confidence: 99%

Is sleep-disordered breathing an additional risk factor for the metabolic syndrome in obese children and adolescents?

et al. 2008

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Sleep-disordered breathing is highly prevalent in childhood obesity. Two recent cross-sectional studies have demonstrated an independent association between the severity of sleep-disordered breathing and the metabolic syndrome. A limited number of studies have also addressed the correlation between sleep-disordered breathing and insulin resistance, the core factor of the metabolic syndrome. Cross-sectional reports in modestly obese children are in favor of an association between sleep apnea and insulin resistance. However, these findings were not confirmed in studies of normal-weight children and of morbidly obese children. Only one out of three treatment studies before and after adenotonsillectomy confirmed the association between sleep apnea and insulin resistance, but only in obese children. Although statistical power issues and differences in patient characteristics might partially explain these contradicting results, the evidence to date is far from establishing a causal link between sleep-disordered breathing and insulin resistance. Longitudinal studies and randomized control trials are therefore warranted to investigate a possible causal link between sleep-disordered breathing and insulin resistance.

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Sleep-Disordered Breathing and the Metabolic Syndrome in Overweight and Obese Children and Adolescents

Cited by 132 publications

References 37 publications

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

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

Weight Loss and Sleep‐Disordered Breathing in Childhood Obesity: Effects on Inflammation and Uric Acid

Is sleep-disordered breathing an additional risk factor for the metabolic syndrome in obese children and adolescents?

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