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Sleep Extension To Reduce Diabetes and Obesity Risk

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Diabetes is a rising epidemic in the U.S., largely attributed to the alarming increase in overweight and obesity. It is believed that the current epidemic of obesity is mainly driven by environmental factors that alter the balance between energy intake and energy expenditure. It is well recognized that the prevention of diabetes and obesity is an attainable goal through modest lifestyle changes aimed at reducing caloric intake, improving food choices and increasing physical activity. Despite substantial resources applied to implement such lifestyle interventions, the economic and public health burden of diabetes and obesity remains enormous. Thus, the identification of potential barriers to success in such effort and the development of novel strategies to prevent or treat diabetes and obesity are critical public health challenges. In parallel with the epidemics of diabetes and obesity, voluntary sleep curtailment has become an increasingly prevalent behavior. Substantial evidence from epidemiologic and laboratory studies suggest that short sleep duration may be an important modulator of diabetes and obesity risk. However, it remains unknown today whether an intervention aimed to increase sleep duration in individuals who habitually curtail their sleep has any beneficial effects on energy metabolism. Our overall goal is therefore to conduct an intervention study in a real life setting to investigate the effects of sleep extension on glucose metabolism and energy balance in habitual short sleepers. We propose a randomized controlled study that will combine objective monitoring of sleep in free-living conditions with the state-of-the-art methods for assessments of insulin sensitivity and beta cell function, body composition, energy intake and food preferences, and all components of energy expenditure. Overweight young adults who habitually sleep less than 6 hours per night (as confirmed by actigraphy) will be studied. After 2-weeks of habitual sleep [baseline] period, subjects will be randomized to either 2-weeks of sleep extension (Extension group, n=40) or 2-weeks of continued habitual sleep (Control group, n=40). We will perform the same procedures during each 2-week sleep period and changes from baseline will be compared between the 2 groups. Our specific aims are to test the hypotheses that: 1) sleep extension will improve insulin sensitivity and beta cell function; 2) sleep extension will reduce average daily energy intake; 3) sleep extension will increase total daily energy expenditure, mainly due to an increase in physical activity. This study will be the first to examine how an intervention aimed to extend sleep duration affects glucose metabolism, energy intake and energy expenditure in a real life setting in individuals who are at risk for diabetes and obesity. These findings may provide important insights to our understanding of the processes underlying the links between sleep and energy metabolism. If the proposed study demonstrates a clear benefit of sleep extension on energy metabolism, these findings may have important implications for the development of novel lifestyle strategies aimed to reduce the burden of current epidemics of obesity and type 2 diabetes, and thus may benefit millions of Americans.
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