LEAP2 and obesity due to melanocortin 4 receptor deficiency: These correlations might suggest the implication of the eCBome, and in particular, of NAEs—which are biosynthesized through GDE1 (among other enzymes) and (like N-acyl-glycines) are degraded by FAAH, and act as agonists at PPARα (as in the case of OEA and PEA, similar to N-acyl-glycines) and PPARγ (as in the case of AEA) and/or antagonists at TRPV2 (as in the case of OEA and N-linoleoyl-ethanolamine [LEA]) [7,24,25]—in Leap2 up-regulation during the development of HFHS-induced glucose intolerance and obesity.