Transkingdom control of microbiota diurnal oscillations promotes metabolic homeostasis.
Level 5 - mechanism / opinion, no new human data
Bench, animal model, and exploratory human mechanistic research.
PubMed 25417104 · doi:10.1016/j.cell.2014.09.048
What was done
The authors examined diurnal variations in gut microbiota composition and function over 24-hour cycles in both mice and humans. They evaluated how feeding rhythms, genetic disruption of the host molecular clock, and jet lag affected microbiome oscillations, and tested whether fecal microbiota transplantation from jet-lagged donors (mice and humans) could transfer metabolic abnormalities into germ-free mice.
What was found
The abstract reports no numerical data, confidence intervals, or specific p-values. Qualitatively, the gut microbiota demonstrated diurnal fluctuations governed by feeding timing; host clock ablation or jet lag disrupted these rhythms and induced dysbiosis; and fecal transfer of this dysbiotic microbiota into germ-free recipient mice caused glucose intolerance and increased adiposity.
Why it matters
This work establishes a mechanistic link between circadian disruption, aberrant microbiome rhythmicity, and metabolic impairment, offering a potential biological explanation for metabolic disorders common in shift workers.
Limits
The abstract provides no sample sizes, effect sizes, or quantitative measurements for any human or animal experiments. The causal link between microbiome disruption and host metabolic phenotypes relies on germ-free mouse transfer models rather than controlled longitudinal human metabolic outcomes.
Cited by
- supports The timing of food intake has an independent effect on the composition and metabolic/circadian function of gut microbes across a 24-hour cycle.
- supports Disrupting circadian microbial rhythmicity via altered feeding patterns or jet lag promotes host susceptibility to obesity and type 2 diabetes.
- supports Time-restricted feeding can completely restore normal microbiome circadian rhythmicity and downstream host metabolic and immune function in jet-lagged or clock-deficient mice.