Journal
BEST PRACTICE & RESEARCH CLINICAL ENDOCRINOLOGY & METABOLISM
Volume 24, Issue 5, Pages 687-702Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.beem.2010.07.005
Keywords
Sleep deprivation; Glucose metabolism; Appetite regulation; Diabetes; Obesity
Categories
Funding
- US National Institute of Health [P01 AG-11412, U54 RR023560, P60 DK-20595, R01 DK-0716960, R01 HL-075025, P50-HD057796]
- US Department of Defense [W81XWH-07-2-0071]
- Belgian CARE Foundation
- INSERM [U628]
- Claude Bernard University of Lyon, France
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Sleep curtailment has become a common behavior in modern society. This review summarizes the current laboratory evidence indicating that sleep loss may contribute to the pathophysiology of diabetes mellitus and obesity. Experimentally induced sleep loss in healthy volunteers decreases insulin sensitivity without adequate compensation in beta-cell function, resulting in impaired glucose tolerance and increased diabetes risk. Lack of sleep also down-regulates the satiety hormone leptin, up-regulates the appetite-stimulating hormone gill-din, and increases hunger and food intake. Taken together with the epidemiologic evidence for an association between short sleep and the prevalence or incidence of diabetes mellitus and/or obesity, these results support a role for reduced sleep duration in the current epidemic of these metabolic disorders. Screening for habitual sleep patterns in patients with diabesity is therefore of great importance. Studies are warranted to investigate the putative therapeutic impact of extending sleep in habitual short sleepers with metabolic disorders. (C) 2010 Elsevier Ltd. All rights reserved.
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