Sleep fragmentation, metabolism, and sleepiness
A model of instrumental sleep fragmentation in mice was introduced and led to an increase in food intake, with no effect on body weight, alterations in brain temperature but not abdominal temperature, as well as increases in corticosterone and a reduced glucose tolerance.
Abstract
Epidemiological evidence for a link betweensleepdurationand obesity has fuelled research aimed at understanding the underlying mechanisms. In humans, sleep restriction, SWS disruption and sleep fragmentation have all been reported to lead to alterations in endocrine and metabolic variables which could mediate the link between sleep disruption and obesity. To better understand the mechanisms, animal models are essential. In the present issue of the Journal, a model of instrumental sleep fragmentation in mice is introduced (Baud et al., 2013). Fourteen days of fragmentation of sleep through rotation of the cage floor was associated with a moderate reduction in total sleep time from613 to 512 min per 24 h anda reduction in the duration of sleep bouts. The intervention led to an increase in food intake, with no effect on body weight, alterations in brain temperature but not abdominal temperature, as well as increases in corticosterone and a reduced glucose tolerance. Comparing the effects of thismodel of sleep disruption to other models, such as the mistimed sleep paradigm in mice (Barclay et al., 2012) or the VLPO lesion induced reduction in sleep duration in rats (Vetrivelan et al., 2012) may uncover some of the mediators of the association between insufficient sleep and disturbance of metabolism. Discrepancies between the results obtained by these various models may also be helpful in characterising when short sleep leads to metabolic changes and when not.