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N-acylethanolamines, anandamide and food intake

N-acylethanolamines, anandamide and food intake

  1. Anonymous
    Biochemical Pharmacology 78 (2009) 553–560
    Harald S. Hansen, Thi Ai Diep

    Anandamide and the other N-acylethanolamines, e.g. oleoylethanolamide (OEA), palmitoylethanolamide
    (PEA), and linoleoylethanolamide (LEA), may be formed by several enzymatic pathways from their
    precursors, which are the N-acylated ethanolamine phospholipids. The exact enzymatic pathways
    involved in their biosynthesis in specific tissues are not clarified. It has been suggested that endogenous
    anandamide could stimulate food intake by activation of cannabinoid receptors in the brain and/or in the
    intestinal tissue. On the other hand, endogenous OEA and PEA have been suggested to inhibit food intake
    by acting on receptors in the intestine. At present, there is no clear role for endogenous anandamide in
    controlling food intake via cannabinoid receptors, neither centrally nor in the gastrointestinal tract.
    However, OEA, PEA and perhaps also LEA may be involved in regulation of food intake by selective
    prolongation of feeding latency and post-meal interval. These N-acylethanolamines seem to be formed
    locally in the intestine, where they can activate PPARa located in close proximity to their site of
    synthesis. The rapid onset of OEA response and its reliance on an intact vagus nerve suggests that
    activation of PPARa does not result in formation of a transcription-dependent signal but must rely on an
    unidentified non-genomic signal that translates to activation of vagal afferents. Whether GPR119, TRPV1
    and/or intestinal ceramide levels also contribute to the anorectic and weight-reducing effect of
    exogenous OEA is less clear.
    Prolonged intake of dietary fat (45 energy%) may promote over-consumption of food by decreasing
    the endogenous levels of OEA, PEA and LEA in the intestine.
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