Table 10.
Endocannabinoid-Like Compounds (Fatty-Acid Ethanolamides) | Biological Effect(s) and/or Mechanism of Action | Reference | |
---|---|---|---|
i. | OEA (an endogenous PPAR-α agonist) |
Via binding to peroxisome proliferators-activate receptor-α (PPAR- α) |
[136] |
ii. | Palmitoylethanolamide (PEA) |
|
[136] |
iii. | N-oleoyl-ethanolamide | May act as an alternative substrate for FAAH, and in doing so, inhibit the degradation of AEA | [383,384] |
iv. | N-linoleoyl-ethanolamide | May act as an alternative substrate for FAAH, and in doing so, inhibit the degradation of AEA | [383,384] |
v. | N-arachidonoyl-glycine | May act as an alternative substrate for FAAH, and in doing so, inhibit the degradation of AEA | [384,385,386] |
vi. | N-acyl-taurine | May act as an alternative substrate for FAAH, and in doing so, inhibit the degradation of AEA | [383,384,387] |
vii. | N-palmitoyl-ethanolamide | Reduced expression of FAAH | [384,388] |