Role of sleep duration in the regulation of glucose metabolism and appetite

Abstract

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 ghrelin, 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.

Figure 1

Self-reported sleep duration (hours) for US and French adults (panels A) and adolescents (panels B). For adolescents, a sleep duration of <8 hours is considered insufficient, from 8 to 9 hours borderline, and ≥9 hours optimal. Adapted from [6-9].

Figure 2

Relationship between sleep duration and the 24h profiles of HOMA, cortisol, growth hormone, leptin and cardiac sympathovagal balance. Adapted from [18, 19]. The bars represent the sleep periods. The shaded area represent the response to breakfast for HOMA and the evening levels for cortisol profiles.