Association between Inadequate Sleep and Insulin Resistance in Obese Children

Flint, Janna K.; Kothare, Sanjeev V.; Zihlif, Mamoon; Suarez, Elizabeth A.; Adams, Ruth; Legido, Agustín; Luca, Francesco De

doi:10.1016/j.jpeds.2006.08.063

Cited by 144 publications

(126 citation statements)

References 35 publications

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“…For instance, children with short sleep duration show decreases in leptin concentrations, decreased insulin sensitivity and altered cortisol concentrations, all promoting lipogenesis. 15,51,52 Thus, changes in hypothalamic functioning, such as altered hypocretin-1 signaling may explain the relationship between the changes in BMI and in sleep duration during puberty, via altered puberty onset, energy balance regulation and circadian rhythm. As food-entrainment in addition to light-entrainment, functions as a 'Zeitgeber' of the circadian rhythm, possibly alterations in dietary patterns may also explain the relationship between BMI and sleep duration.…”

Section: Discussionmentioning

confidence: 99%

“…10,11 Additionally, short sleep duration in children was related to insulin resistance, a larger body fat percentage, a larger waist circumference, decreased physical activity and increased television watching. [12][13][14][15][16] Longitudinal studies have shown that when young children (prepubertally, up to age 12 years) sleep fewer hours per night, they are at a higher risk to become overweight at a later age, during childhood as well as adulthood. [17][18][19][20][21] Sleep duration during childhood, however, naturally decreases, in particular during puberty when a reduction of about 2 h is observed.…”

Section: Introductionmentioning

confidence: 99%

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Sleep duration and body-weight development during puberty in a Dutch children cohort

et al. 2010

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Background: Short sleep duration is associated with obesity during childhood and adulthood. Objective: The objective of our study was to investigate the relationship between sleep duration and body mass index (BMI) from Tanner stages 1 to 5 in a Dutch children cohort. Design: In 98 children, anthropometric measurements and leptin concentrations were measured from age 7 to 16 years; body composition, physical activity (Baecke questionnaire), hours television viewing and self-reported sleep duration were measured yearly from age 12 to 16 years. Moreover, the polymorphisms of the FTO gene (rs9939609) and parental BMI's were determined. Results: At Tanner stages 1-5 sex differences were observed in height, body weight, waist circumference, fat mass per squared meter height and leptin concentrations per kg fat mass. Inverse relationships were observed between the change in BMI (kg m -2 ) and the change in hours of sleep per night (h) from Tanner stages 1 to 4 (r ¼ À0.68, Po0.001), from Tanner stages 2 to 5 (r ¼ À0.35, Po0.05) and from Tanner stages 1 to 5 (r ¼ À0.33, Po0.05). Univariate analysis of variance showed that with progressive Tanner stages, BMI increases and sleep duration decreases in an interrelated way independent of possible confounders (R 2 ¼ 0.38, Po0.02). Conclusion: Changes in BMI during puberty were inversely related to changes in sleep duration, independent of possible confounders.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Sleep duration and body-weight development during puberty in a Dutch children cohort

et al. 2010

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“…However, preliminary data obtained in a small population of children showed that sleep duration was inversely associated with insulin resistance (Flint et al, 2007).…”

Section: Introductionmentioning

confidence: 97%

Determinants and impact of sleep duration in children and adolescents: data of the Kiel Obesity Prevention Study

et al. 2008

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Background/Objectives: This study investigates determinants of sleep duration and its impact on nutritional status, resting energy expenditure (REE), cardiometabolic risk factors and hormones in children/adolescents. Subjects/Methods: In 207 girls and 207 boys (13.0±3.4 (6.1-19.9) years) body mass index standard deviation score (BMI SDS), waist circumference (WC) z-score, body composition (air-displacement plethysmography), REE (ventilated hood system; n ¼ 312) and cardiometabolic risk factors/hormones (n ¼ 250) were assessed. Greater than 90th percentile of BMI/WC references was defined as overweight/overwaist. Sleep duration, media consumption (TV watching/computer use), physical activity, dietary habits, parental BMI, socio-economic status and early infancy were assessed by questionnaire. Short sleep was defined as o10 h per day for children o10 years and otherwise o9 h per day. Results: Total 15.9% participants were overweight, mean sleep duration was 8.9±1.3 h per day. Age explained most variance in sleep (girls: 57.0%; boys: 41.2%) besides a high nutrition quality score (girls: 0.9%) and a low media consumption (boys: 1.3%). Sleep was inversely associated with BMI SDS/WC z-score (girls: r ¼ À0.17/À0.19, Po0.05; boys: r ¼ À0.21/À0.20, Po0.01), which was strengthened after adjusting for confounders. Short vs long sleep was associated with 5.5-/2.3-fold higher risks for obesity/overwaist (girls). After adjusting for age, REE (adjusted for fat-free mass) was positively associated with sleep in boys (r ¼ 0.16, Po0.05). Independently of age and WC z-score, short sleep was associated with lower adiponectin levels in boys (11.7 vs 14.4 mg/ml, Po0.05); leptin levels were inversely related to sleep in girls (r ¼ À0.23, Po0.05). Homoeostasis model assessment-insulin resistance (r ¼ À0.20, Po0.05) and insulin levels (r ¼ À0.20, Po0.05) were associated with sleep (girls), which depended on WC z-score. Conclusions: Age mostly determined sleep. Short sleep was related to a higher BMI SDS/WC z-score (girls/boys), a lower REE (boys), higher leptin (girls) and lower adiponectin levels (boys).

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“…These associations with fasting insulin were confirmed by Li et al 33 and Redline et al, 28 both of whom found that a diagnosis of sleep-disordered breathing was associated with higher insulin concentrations. Flint et al 23 studied 40 obese children. Of these children, 32 had OSAS.…”

Section: Sleep-disordered Breathing and Insulin Resistancementioning

confidence: 99%

“…[16][17][18] Other mechanisms by which sleep-disordered breathing may disturb metabolic control include increased sympathetic activity, 19 higher serum cortisol, 20 increased leptin levels 21 and impaired glucose tolerance and appetite regulation, resulting from secondary sleep debt. [22][23][24] Furthermore, intermittent hypoxia even in lean mice has been shown to induce insulin resistance. 25 In this review, we will provide a concise overview of the current evidence regarding the association between sleepdisordered breathing and the metabolic syndrome in children and adolescents.…”

Section: Introductionmentioning

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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Association between Inadequate Sleep and Insulin Resistance in Obese Children

Cited by 144 publications

References 35 publications

Sleep duration and body-weight development during puberty in a Dutch children cohort

Sleep duration and body-weight development during puberty in a Dutch children cohort

Determinants and impact of sleep duration in children and adolescents: data of the Kiel Obesity Prevention Study

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

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