Sleep influences on obesity, insulin resistance, and risk of type 2 diabetes
Introduction
Approximately one third of human's lifetime is spent sleeping. Sleep is a state of energy restoration and replenishment. In modern society, bedtime is often curtailed to meet increasing personal and social demands. In the United States, self-reported sleep duration has declined over the last 2–3 decades [1]. The epidemics of obesity and diabetes developed simultaneously. Evidence from large cross sectional and longitudinal epidemiologic studies, discussed elsewhere in detail in other articles in this series, demonstrated that insufficient sleep is a risk factor for obesity and diabetes [2,3]. Moreover, poor sleep quality has been linked to similar detrimental effects [3]. To elucidate potential causal mechanisms, this review will focus on the findings from laboratory studies involving the impact of experimental sleep manipulations, including sleep restriction, fragmentation and sleep extension on the control of energy balance and/or glucose metabolism.
Section snippets
Sleep Restriction and Obesity Risk
Outcome measures in laboratory studies addressing the impact of sleep restriction on obesity risk have included assessments of circulating levels of appetite-regulating hormones, self-reports of hunger and appetite, objectively assessed food intake, energy expenditure, weight changes and neuronal activity in specific brain regions. Fig. 1 illustrates our current understanding of pathways linking sleep restriction to obesity risk.
Sleep Restriction and Glucose Metabolism
To date, there have been at least 14 studies addressing the effects of sleep restriction on glucose metabolism [20,30,31,48,[50], [51], [52], [53], [54], [55], [56], [57], [58], [59]]. In a landmark study published in 1999, Spiegel et al. investigated the effects of six nights of 4-h sleep restriction on glucose metabolism assessed by intravenous glucose tolerance testing (IVGTT) [50]. Compared with a fully rested condition achieved using 12-h TIB, 4-h sleep restriction resulted in a 24%
Sleep Fragmentation and Glucose Metabolism
Three studies have utilized the technique of slow wave sleep (SWS) suppression for 1–3 nights to explore the metabolic effects of sleep fragmentation [[63], [64], [65]] (data summarized in Fig. 3). Using acoustic stimuli, Tasali et al. demonstrated that SWS suppression without changes in sleep duration for three nights resulted in a reduction in insulin sensitivity by 25% and glucose tolerance by 23% as assessed by IVGTT [65]. There was also a concomitant increase in cardiac sympatho-vagal
Mechanisms Linking Sleep Restriction and Abnormal Glucose Metabolism
As briefly mentioned above, several pathways could contribute to abnormal glucose metabolism as a result of sleep restriction (Fig. 4). Brain glucose utilization was found to be significantly decreased during total sleep deprivation [66] and a similar mechanism may have contributed to the finding of decreased glucose effectiveness found in the 1999 sleep debt study [50]. Consistently, researchers have shown an increase in sympathetic nervous system activity during sleep restriction or
Metabolic Effects of Optimizing Sleep Duration
In the present section, we summarize emerging evidence suggestive of potential benefits of extending sleep duration in individuals who curtail their habitual sleep. Because of the paucity of studies, we include studies under real life conditions.
Summary
Through well-designed experimental sleep manipulations, researchers have provided convincing evidence that insufficient sleep is a risk factor for obesity, insulin resistance and type 2 diabetes. The body of evidence on the impact of sleep fragmentation is much smaller but is consistent with an adverse effect on diabetes risk. Emerging data suggest that optimizing sleep duration and quality may have beneficial metabolic effects. Pilot studies suggest that sleep extension in habitual short
Conflict of Interest
S.R. receives honoraria from Sanofi Aventis, Medtronic and Novo Nordisk, investigator-initiated research grant from Merck Sharp and Dohme, and research equipment support from ResMed, Thailand.
E.V.C. is a consultant for Philips Medical and Vanda Pharmaceuticals and receives investigator-initiated grant support from Astra-Zeneca, Merck and Shire.
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