Sleep apnea affects nearly one billion people worldwide and causes repeated episodes of oxygen deprivation during the night, known as intermittent hypoxia.
These results shed light on a previously little-known aspect of the disease and could help to better target the optimal time for administering treatments to improve their effectiveness.
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While the pathological consequences of intermittent hypoxia in sleep apnea are well documented, their impact on the body's biological rhythms, governed by the circadian clock, remains poorly explored.
In this study, scientists used a murine model of chronic intermittent hypoxia to analyze, over the entire day-night cycle, the effects of this respiratory stress on the body. By focusing on the liver, a central organ in energy regulation, they combined transcriptomic, metabolomic, and physiological approaches to track the adaptations of hepatic metabolic activity over time.
The results show that intermittent hypoxia not only impairs some major energy pathways orchestrated by the liver, such as glucose and lipid metabolism, but also profoundly reprograms their circadian organization. For example, metabolomic analysis reveals that nearly half of liver metabolites exhibit a 24-hour rhythm and that more than one-third of them acquire a new rhythm under intermittent hypoxia.
This redistribution of metabolic rhythms throughout the day reflects a true temporal reprogramming of hepatic activity and highlights a previously underestimated dimension of sleep apnea.
This work thus opens new perspectives in chronomedicine. By reprogramming the liver's metabolic rhythms, intermittent hypoxia could alter the body's response to certain drugs, particularly those acting on blood sugar or lipid metabolism.
Their effectiveness could therefore vary depending on the time of day, with optimal administration times different from those observed in people without this respiratory disorder. This underscores the importance of integrating the temporal dimension into the management of sleep apnea.