Short sleep duration and obesity: Mechanisms and future perspectives

Departamento de Psicobiologia, Universidade Federal de São Paulo, São Paulo, Brazil.
Cell Biochemistry and Function (Impact Factor: 2.01). 08/2012; 30(6):524-9. DOI: 10.1002/cbf.2832
Source: PubMed


A reduction of sleep time has become common over the last century, and growing evidence from both epidemiological and laboratory-based studies suggests sleep curtailment is a new risk factor for the development of obesity. On this basis, the present review examines the role of sleep curtailment in the metabolic and endocrine alterations, including decreased glucose tolerance and insulin sensitivity, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin and increased hunger and appetite. It will be discussed how sleep restriction may lead to increase in food intake and result in greater fatigue, which may favour decreased energy expenditure. Altogether, evidences point to a possible role of decreased sleep duration in the current epidemic of obesity and therefore present literature highlights the importance of getting enough good sleep for metabolic health. Many aspects still need to be clarified and intervention studies also need to be conducted.

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    • "In Japan, obesity is defined by a BMI of 25 kg/m 2 or over (The Examination Committee of Criteria for 'Obesity Disease' in Japan, 2002); 28.6 % of men and 20.6 % of women, with a BMI of 25 kg/m 2 or over, are defined as obese (Yatsuya et al. 2011). Obese people have an increased incidence of cardiovascular, renal, and hormonal diseases; it is well known that obese people have shortened sleep durations (Zimberg et al. 2012). Sleep deprivation affects endocrine function (Scheen and Van Cauter 1998), such as glucose concentrations and insulin secretion, which lead to an increase in the risk of obesity and diabetes in humans (Buxton et al. 2012). "
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    ABSTRACT: During the past several decades, obesity has been increasing globally. In Japan, obesity is defined by a BMI of 25 kg/m(2) or over; 28.6 % of men and 20.6 % of women are obese. Obese people have an increased incidence of developing cardiovascular, renal, and hormonal diseases and sleep disorders. Obese people also have shortened sleep durations. We investigated seasonal differences in melatonin concentrations, heart rates, and heart rate variability during sleep in obese subjects in Japan. Five obese (BMI, 32.0 ± 4.9 kg/m(2)) and five non-obese (BMI, 23.2 ± 2.9 kg/m(2)) men participated in this study in the summer and winter. Electrocardiograms were measured continuously overnight in a climatic chamber at 26 °C with a relative humidity of 50 %. Saliva samples for melatonin were collected at 2300 hours, 0200 hours, and 0600 hours. We found that melatonin concentrations during sleep in obese subjects were significantly lower than those in non-obese subjects in the winter. Heart rate during sleep in winter was significantly higher than that in summer in both obese and non-obese subjects. Heart rate variability was not significantly different in the summer and winter in both obese and non-obese subjects. Our results show that decreased nocturnal melatonin concentrations during winter in obese men may be related to higher heart rates, and this may suggest that obese men are at an increased risk of a cardiovascular incident during sleep, especially in the winter.
    International Journal of Biometeorology 10/2012; 57(5). DOI:10.1007/s00484-012-0601-3 · 3.25 Impact Factor
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    • "Future interventional studies of sleep duration and metabolism over longer periods while participants are living in their normal environment are warranted. If these studies yield positive results the findings could be translated into lifestyle " sleep " advice for obese people and patients [46] "
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    ABSTRACT: Objectives: Evidence for a causal relationship between sleep-loss and metabolism is derived primarily from short-term sleep deprivation studies in the laboratory. The objective of this study was to investigate whether small changes in sleep duration over a three week period while participants are living in their normal environment lead to changes in insulin sensitivity and other metabolic parameters. Methods: Nineteen healthy, young, normal-weight men were randomised to either sleep restriction (habitual bedtime minus 1.5h) or a control condition (habitual bedtime) for three weeks. Weekly assessments of insulin sensitivity by hyperinsulinaemic-euglycaemic clamp, anthropometry, vascular function, leptin and adiponectin were made. Sleep was assessed continuously using actigraphy and diaries. Results: Assessment of sleep by actigraphy confirmed that the intervention reduced daily sleep duration by 01:19 ± 00:15 (SE; p<0.001). Sleep restriction led to changes in insulin sensitivity, body weight and plasma concentrations of leptin which varied during the three week period. There was no effect on plasma adiponectin or vascular function. Conclusions: Even minor reductions in sleep duration lead to changes in insulin sensitivity, body weight and other metabolic parameters which vary during the exposure period. Larger and longer longitudinal studies of sleep restriction and sleep extension are warranted.
    Metabolism: clinical and experimental 09/2012; 62(2). DOI:10.1016/j.metabol.2012.07.016 · 3.89 Impact Factor
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