Tier 4 — mechanistic

Feline drug metabolism and disposition: pharmacokinetic evidence for species differences and molecular mechanisms

Court MH
Veterinary Clinics of North America: Small Animal Practice 2013 43(5):1039-1054

Bibliography

PubMed
PMID 23890237

Study snapshot

DesignNarrative review
ModelReview of feline comparative pharmacokinetics and drug-metabolising enzyme deficiencies
SampleNot applicable — literature review, no original experimental sample.
InterventionNot applicable — narrative review of feline drug metabolism; no fisetin experiment.
DurationNot applicable — literature synthesis without new animal or human follow-up.
EndpointsFeline drug-metabolizing enzyme activity; UGT-dependent glucuronidation and species differences; Drug disposition and toxicity implications

What the study showed, in plain terms

This review explains that cats process many drugs and dietary compounds differently from dogs and humans because they lack functional UGT1A6, a liver enzyme most mammals use to clear phenolic compounds (including paracetamol, aspirin, and many plant compounds) via glucuronidation. This is why cats are unusually sensitive to certain drugs and why doses calculated for dogs or humans cannot simply be scaled down for cats.

Key findings

Cats have a well-documented deficiency in UGT (UDP-glucuronosyltransferase) enzyme activity, particularly UGT1A6, which is functionally inactive in domestic cats and other Felidae. This explains feline sensitivity to paracetamol, aspirin, propofol, and other glucuronidation-dependent compounds. Does not test fisetin or any flavonoid specifically.

What this study can and cannot tell us

Narrative review, not primary data. Does not address fisetin or flavonoid pharmacokinetics specifically — use only to explain the general mechanism of feline glucuronidation deficiency.

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