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Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...
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Clock-modulated checkpoints in time-restricted eating.

Min-Dian Li1

  • 1Department of Cardiology and the Center for Circadian Metabolism and Cardiovascular Disease, Southwest Hospital, Army Medical University, Chongqing, 400038, China.

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|November 21, 2021
PubMed
Summary
This summary is machine-generated.

Time-restricted eating (TRE) helps prevent cardiometabolic diseases by aligning body rhythms. New research suggests TRE uses clock-modulated checkpoints (CCPs) to reset tissue functions, offering precision medicine potential.

Keywords:
cardiometabolic diseasescircadian rhythmde novo lipogenesismetabolic dysfunction-associated fatty liver diseaseperipheral clockstime-restricted eating

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Area of Science:

  • Chronobiology
  • Metabolic disease research
  • Physiology

Background:

  • Time-restricted eating (TRE) involves consuming meals within a 6-12 hour daily window.
  • TRE is associated with reduced cardiometabolic disease risk by synchronizing metabolic and physiological circadian rhythms.
  • Canonical circadian clocks are not essential for TRE's effects in the liver, indicating tissue-specific entrainment.

Purpose of the Study:

  • To propose that TRE utilizes clock-modulated checkpoints (CCPs) to reset circadian rhythms in tissues.
  • To investigate the mechanistic basis of tissue responsiveness to TRE.
  • To facilitate the application of TRE in precision medicine for cardiometabolic diseases.

Main Methods:

  • Investigating the role of clock-modulated checkpoints (CCPs) in TRE.
  • Analyzing tissue-specific entrainment of circadian rhythms by meal timing.
  • Examining the dispensability of canonical circadian clocks for TRE's metabolic actions.

Main Results:

  • TRE's effects are independent of canonical circadian clocks in certain tissues like the liver.
  • Peripheral tissues exhibit differential entrainability to meal timing (e.g., liver and fat are responsive; heart and kidneys are resistant).
  • A proposed mechanism involves TRE engaging CCPs to reset tissue circadian rhythms.

Conclusions:

  • TRE resets circadian rhythms through tissue-specific mechanisms, potentially involving CCPs.
  • Understanding CCPs is crucial for elucidating TRE's impact on metabolic health.
  • This research paves the way for personalized TRE interventions in managing cardiometabolic diseases.