Time-restricted eating improves intermittent hypoxia-induced dysglycemia.
Chloe P Afif1, Katherine P Brewster2, Michelle P Zhang3
1Department of Molecular, Cellular, and Developmental Biology, University of California Santa Barbara, Santa Barbara, CA, United States.
Sleep
|November 25, 2025
Summary
Time restricted eating (TRE) mitigates glucose dysregulation caused by intermittent hypoxia (IH), a model for obstructive sleep apnea (OSA). TRE improves insulin secretion and may be a novel therapeutic strategy for OSA.
Area of Science:
- Metabolic Physiology
- Sleep Medicine
- Endocrinology
Background:
- Obstructive sleep apnea (OSA) is linked to abnormal glucose metabolism.
- Chronic intermittent hypoxia (IH), mimicking OSA, induces similar metabolic disturbances.
- Time restricted eating (TRE) shows metabolic benefits, but its effect on IH-induced dysglycemia in obesity is unclear.
Purpose of the Study:
- To investigate the efficacy of TRE in improving glucose homeostasis in an obese rodent model of OSA exposed to IH.
- To determine if TRE can counteract IH-induced dysglycemia and associated metabolic changes.
Main Methods:
- Obese C57BL/6J mice on a high-fat diet were exposed to either intermittent air (IA) or IH for four weeks.
- Mice were assigned to either ad libitum feeding or TRE (9h/d intake).
- Glucose tolerance tests (GTT) were conducted before and after the exposure period.
Main Results:
- TRE significantly reduced fasting glucose in the IH group compared to controls.
- TRE prevented the increase in glucose tolerance test area under the curve observed in both IA and IH ad libitum groups.
- TRE normalized elevated serum proinsulin and proinsulin-to-insulin ratios in IH mice, with favorable pancreatic gene expression changes.
Conclusions:
- TRE effectively mitigates the adverse effects of IH on glucose homeostasis, primarily by improving pancreatic insulin secretion.
- The glucose-regulating benefits of TRE are enhanced under IH conditions.
- TRE presents a potential therapeutic approach for managing metabolic dysfunction in OSA.
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