Palmitoylethanolamide (PEA) as well as the other N-acylethanolamines (NAEs), e.g. anandamide,
oleoylethanolamide, stearoylethanolamide and linoleoylethanolamide, appear to exist in every mammalian cell at low
levels, e.g. a few hundred pmol/g tissue for PEA. Their formation can be stimulated by cellular injury and inflammation.
In the brain PEA and other NAEs may have neuroprotective functions. PEA levels in tissues seem hardly to be influenced
by variation in intake of dietary fatty acids, except in the small intestine where dietary fat results in decreased levels of
PEA and other NAEs. In rat small intestine, PEA, oleoylethanolamide and linoleoylethanolamide have anorectic
properties. Of other dietary components, only ethanol is known to influence tissue levels of PEA. Thus, an acute
intoxicating dose of ethanol will decrease PEA levels in various areas in the brain of rats. The mechanism behind this
effect is not known.
Keywords: N-acylethanolamines, dietary fat, ethanolamine, ethanol, tissue levels, rat, human
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