Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2008) 16 PL7

When and why do we wake up – the endocrine regulation of sleep in humans

Decreased sleep duration and quality: novel risk factors for obesity and diabetes

Eve Van Cauter

The University of Chicago, Chicago, Illinois, USA.

Sleep curtailment has become a common behavior in industrialized countries. Simultaneously, the aging of the population is associated with an increased prevalence of sleep disturbances. These trends for shorter sleep duration and poorer sleep quality have developed over the same time period as the dramatic increase in the prevalence of obesity and diabetes. There is recent evidence to indicate that chronic partial sleep loss and decreased sleep quality may increase the risk of obesity and diabetes. Studies in healthy volunteers have shown that sleep restriction (4–6 h bedtimes) is associated with an adverse impact on glucose homeostasis. Insulin sensitivity decreases rapidly and markedly without adequate compensation in beta cell function, resulting in an elevated risk of diabetes. Multiple factors appear to mediate this adverse impact of sleep loss, including increased sympathetic nervous activity, decreased brain glucose uptake and elevated evening cortisol levels. Reduced sleep quality, without change in sleep duration, is also associated with an increased risk of diabetes. Indeed, selective suppression of slow-wave sleep, a highly heritable trait, rapidly results in a marked reduction in insulin sensitivity and disposition index. Prospective epidemiologic studies in children and adults are consistent with a role for sleep disturbances in the increased risk of diabetes. Sleep curtailment is also associated with a dysregulation of the neuroendocrine control of appetite. Under conditions of controlled caloric intake and energy expenditure, there is a negative relationship between leptin levels and sleep duration. In a randomized cross-over design study (2 days of 4-h versus 8-h bedtimes), leptin levels were decreased and ghrelin levels increased during the short sleep condition, and the change in the ghrelin to leptin ratio was strongly correlated with increased hunger. Thus, sleep loss may alter the ability of leptin and ghrelin to accurately signal caloric need. Consistent with the laboratory evidence, epidemiologic studies have shown an association between short sleep and higher BMI after controlling for a variety of possible confounders. Taken together, the current evidence suggest that chronic partial sleep curtailment, a novel behavior that appears to have developed with the advent of the 24-h society, and reduced sleep quality may be involved in the current epidemic of obesity and diabetes.

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