Artículos de revistas
A link between sleep loss, glucose metabolism and adipokines
Fecha
2011-10-01Registro en:
Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 44, n. 10, p. 992-999, 2011.
0100-879X
S0100-879X2011001000003.pdf
S0100-879X2011001000003
10.1590/S0100-879X2011007500113
WOS:000295721600003
Autor
Padilha, Heloisa Vidigal Guarita
Crispim, Cibele Aparecida
Zimberg, Ioná Zalcman
Souza, Daurea Abadia de
Waterhouse, Jim Maris
Tufik, Sergio
Mello, Marco Tulio de
Institución
Resumen
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.