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2015). These studies, taken together, advise that, although a direct activation of GPR55 or PPAR‐α takes place, PEA can create its anti‐inflammatory action during the gut also through indirect activation of CB1 and CB2 receptors, in all probability because of the flexibility of the compound to potentiate the action of endocannabinoids at these
2016a). This scaled-down enhance was proportionate to the smaller peak of PEA ranges detected in human volunteers when compared with beagle canines. This variation, subsequently, can be caused by the decreased overall number of PEA acutely administered to human volunteers (about ∼five vs. 30 mg·kg−one in canine) and to The point that this was