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Time-Restricted Feeding Reinforces Gut Rhythmicity by Restoring Rhythms in Intestinal Metabolism in a Jetlag Mouse
Hui Leng1, Theo Thijs1, Louis Desmet1
1Translational Research Center in Gastrointestinal Disorders (TARGID), KU Leuven, Leuven, Belgium.
Cellular and Molecular Gastroenterology and Hepatology
|December 12, 2024
Summary
Time-restricted feeding (TRF) helps realign disrupted circadian rhythms in the jejunum caused by chronic jetlag. This study shows TRF rescues metabolic and cellular organization pathways, improving gut health.
Area of Science:
- Chronobiology
- Gastroenterology
- Molecular Biology
Background:
- Circadian rhythm disruptions, such as chronic jetlag, negatively impact health, leading to gastrointestinal issues.
- The jejunal mucosa's physiological pathways are affected by circadian disturbances.
Purpose of the Study:
- To investigate physiological pathways in jejunal mucosa disrupted by chronic jetlag.
- To determine if time-restricted feeding (TRF) can prevent these disruptions.
- To utilize mouse enteroids to model jejunal epithelial clock-dependent processes.
Main Methods:
- Mice were subjected to chronic jetlag or night-time TRF for 4 weeks.
- Bulk RNA sequencing of jejunal mucosa was performed to analyze transcriptomic changes.
- Bmal1 wild-type and knockout mouse enteroids were generated to study clock dependency.
Main Results:
- Chronic jetlag disrupted jejunal clock gene rhythmicity and the overall transcriptome, with partial rescue by TRF.
- TRF prevented jetlag-induced alterations in genes related to nutrient transport, lipid metabolism, ketogenesis, and cellular organization.
- In vivo, TRF prevented jetlag-induced phase shifts in neutral lipid accumulation and diurnal crypt cell proliferation rhythms.
Conclusions:
- Time-restricted feeding (TRF) effectively entrains circadian rhythms in the jejunal mucosa during chronic jetlag.
- TRF realigns metabolic and cellular organization pathways disrupted by jetlag.
- Jejunal enteroids serve as a viable in vitro model for studying clock-dependent lipid metabolism.
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