A link between sleep loss, glucose metabolism and adipokines

The present review evaluates the role of sleep and its alteration in triggering problems of glucose metabolism and the possible involvement of adipokines in this process. A reduction in the amount of time spent sleeping has become an endemic condition in modern society, and a search of the current literature has found important associations between sleep loss and alterations of nutritional and metabolic contexts. Studies suggest that sleep loss is associated with problems in glucose metabolism and a higher risk for the development of insulin resistance and type 2 diabetes mellitus. The mechanism involved may be associated with the decreased efficacy of regulation of the hypothalamus-pituitary-adrenal axis by negative feedback mechanisms in sleep-deprivation conditions. In addition, changes in the circadian pattern of growth hormone (GH) secretion might also contribute to the alterations in glucose regulation observed during sleep loss. On the other hand, sleep deprivation stress affects adipokines - increasing tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) and decreasing leptin and adiponectin -, thus establishing a possible association between sleep-debt, adipokines and glucose metabolism. Thus, a modified release of adipokines resulting from sleep deprivation could lead to a chronic sub-inflammatory state that could play a central role in the development of insulin resistance and type 2 diabetes mellitus. Further studies are necessary to investigate the role of sleep loss in adipokine release and its relationship with glucose metabolism.

Circadian rhythms in the neonate and in old age: what do they tell us about the development and decay of the body clock in humans?

This overview describes changes in human circadian rhythms in the neonate and in aged subjects. Since a measured circadian rhythm is derived from an endogenous (clock-driven) component and an erogenous component (due to rhythms in the environment and lifestyle), this account attempts to separate these possibilities in any particular case. Experimental methods for distinguishing between these components are described, and it is concluded that the data are rarely clear enough for such distinctions in mechanism to be made with confidence. Nevertheless, the evidence to date suggests that changes to the endogenous and exogenous components during both the development and decay of circadian rhythms are involved. This being the case, and accepting that poorly developed circadian rhythms are often associated with poor general health and development, methods to strengthen circadian rhythms are described.