Associations between sleep loss and increased risk of obesity and diabetes

Abstract

During the past few decades, sleep curtailment has become a very common in industrialized countries. This trend for shorter sleep duration has developed over the same time period as the dramatic increase in the prevalence of obesity and diabetes. Evidence is rapidly accumulating to indicate that chronic partial sleep loss may increase the risk of obesity and diabetes. Laboratory studies in healthy volunteers have shown that experimental sleep restriction 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. Prospective epidemiologic studies in both children and adults are consistent with a causative role of short sleep in the increased risk of diabetes. Sleep curtailment is also associated with a dysregulation of the neuroendocrine control of appetite, with a reduction of the satiety factor, leptin, and an increase in the hunger-promoting hormone, ghrelin. Thus, sleep loss may alter the ability of leptin and ghrelin to accurately signal caloric need, acting in concert to produce an internal misperception of insufficient energy availability. The adverse impact of sleep deprivation on appetite regulation is likely to be driven by increased activity in neuronal populations expressing the excitatory peptides orexins that promote both waking and feeding. Consistent with the laboratory evidence, multiple epidemiologic studies have shown an association between short sleep and higher body mass index after controlling for a variety of possible confounders.

Figure 1

Schematic of the putative pathways leading from sleep loss to diabetes and obesity risk.

Figure 2

Schematic of the Orexin System. TMN: tuberomammillary nucleus; NTS: nucleus tractus solitaries; PVN: paraventricular nucleus; VTA: ventro-tegmental area; NA: nucleus accumbens (NA). Grey arrows represented stimulatory (+) pathways and black dashed lines reflect inhibitory (−) pathways.

Figure 3

Profiles of hunger ratings, appetite ratings and the ghrelin-to-leptin ratio during the long sleep (10 hour) and short sleep (4 hour) conditions in a single representative subject.