It is the study of how intra- and inter-individual differences in the bacteria associated with us especially gut bacteria (aka gut microbiota) affect drug response – leading to different effectiveness and safety outcomes.
An important question arises: How can we dissect the contributions of gut microbiota versus human host metabolism to the temporal handling of drug in our body (aka pharmacokinetics)?
To achieve this goal, Zimmermann and colleagues combined genetic makeup of gut bacteria with mouse model of known gut bacteria (aka gnotobiotics) to measure metabolism of anti-shingle drug (aka brivudine) in mice that vary in a single bacterial (microbiome-encoded) enzyme.
Informed by these measurements, they built a pharmacokinetic model to quantitatively predict gut bacterial contributions to levels of the drug and its metabolite in blood over time.
Of course, in the spirit of solid scientific inquiry, additional study on an antidepressant drug (clonazepam) with multiple metabolism pathways was further performed to prove that this approach could be applied to other drugs.
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