In modern society, sleep duration has decreased with concurrent increase in cardiometabolic and neurological diseases. It is said that lack of sleep can increase the risk for development of such disorders; however, a clear molecular link is yet to be established. Metabolomics, the study of metabolites, has been used for an extensive understanding of molecular mechanisms of diseases and may shed light to molecular effects of sleep curtailment. To this end, previous studies have shown elevation of phospholipids after sleep restriction in both human and rat species, as well as metabolites associated with an oxidizing environment. This provides a potential link between known pathologies of reduced sleep duration and metabolic dysfunction. At a behavioral level, sleep deprivation (SD) has been shown to negatively influence attention, brain activation, and cognition, with potentially fatal consequences. Interestingly, interindividual differences are manifested in such neurobehavioral response post SD as suggested by psychomotor vigilance task (PVT). It has been discovered that individuals who are resistant to the effects of SD are likely to have more robust compensatory mechanisms to sustain wakefulness than the subjects behaviorally sensitive to the effects of SD. To further understand this effect, we recruited extremely sensitive (N=10, PVT score 0.61 ± 0.51) and extremely resistant (N = 10, 0.05 ± 0.04) subjects and profiled their blood plasma using NMR spectroscopy. Preliminary results suggest differential effects on energy metabolism and branched-chain amino acid catabolism across the groups. Further data acquisition and analysis are ongoing and will provide more insight.

Biomarkers of sleep-loss vulnerability and total sleep deprivation by metabolomics

2019 Spring National Meeting

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