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Gut Microbe-Derived Trimethylamine Shapes Circadian Rhythms Through the Host Receptor TAAR5
Kala K Mahen1,2,3, William J Massey2,4, Danny Orabi1
1Department of Cancer Biology, Cleveland Clinic, Cleveland, OH 44195, USA.
Biorxiv : the Preprint Server for Biology
|November 24, 2025
Summary
Trimethylamine (TMA), a gut microbe metabolite, influences host circadian rhythms and metabolic health. Targeting the TMA receptor (TAAR5) reveals new diet-microbe-host interactions relevant to cardiometabolic disease.
Area of Science:
- Microbiology
- Metabolism
- Chronobiology
Background:
- Gut microbe-derived trimethylamine N-oxide (TMAO) is linked to cardiometabolic disease risk.
- The mechanisms connecting TMAO production to human disease remain unclear.
- Dietary choline is converted to trimethylamine (TMA) by gut bacteria, then oxidized to TMAO by the host.
Purpose of the Study:
- To investigate whether the primary metabolite TMA, rather than TMAO, impacts host metabolic homeostasis and circadian rhythms.
- To explore the role of the host receptor trace amine-associated receptor 5 (TAAR5) in mediating TMA's effects.
Main Methods:
- Utilized knockout mice lacking the TAAR5 receptor (Taar5-/-).
- Examined mice genetically deficient in bacterial TMA production or host TMA oxidation.
- Assessed circadian rhythms in gene expression, metabolic hormones, gut microbiome, and behavior.
Main Results:
- Mice lacking TAAR5 exhibited altered circadian rhythms in gene expression, metabolic hormones, gut microbiome, and behavior.
- Disruptions in bacterial TMA production or host TMA oxidation also led to altered circadian rhythms.
- These findings highlight TMA's role in regulating circadian physiology.
Conclusions:
- Gut bacterial production of TMA and host sensing via TAAR5 are implicated in the physiological regulation of circadian rhythms in mice.
- These findings offer novel insights into diet-microbe-host interactions relevant to cardiometabolic disease.
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