Fatty acid Ethanolamides: a claim to fight against obesity

Fatty Acid Ethanolamides

  • Fatty acid ethanolamides belong to a family of lipid naturally found in both plant and animal tissues. These fatty acid derivatives appear to have biological properties.
  • Palmitoylethanolamide (PEA, derived from palmitic acid) has anti-nonciceptive and anti-inflammatory properties.
  • Anandamide (derived from arachidonic acid) is an endogenous ligand for cannabinoid receptor subtype 1 (CB1) .by activating this receptor, anandamide, increases food intake.
  • Oleoylethanolamide, formed from oleic acid and phosphatidylethanolamine has following biological Function
    • To control food intake through activation of peripheral PPAR-  α
    • To promote lipid utilization
    • To modulate lipid storage in liver and circulating plasma lipids (triglycerides and cholesterol)


Oleoylethanolamide and food intake control
 


This molecule is naturally present at low concentration in food products such as cocoa powder (up to 2 µg/g), oatmeal or nuts. Biologically, the OEA function is to regulate food intake via synthesis/degradation balance, which occur mainly in the enterocytes (brush border).  OEA is synthesized in he small intestine of various vertebrate species. Its level decreases during starvation and increases upon re-feeding.  Food intake may stimulate N-acyltransferase (NAT) activity, and biosynthesized OEA can trigger satiety signals.

  • Pharmacological studies shows that there is a significant decrease of food intake for 4 hr after intraperitoneal (ip) injection OEA at 5mg/ kg of body wt and for all of the 9 days  of the experimenting rats.
  • Compared to the control, the percentage of food intake decrease were 32, 24 and 14% respectively for 20, 10 and 5 mg OEA/kg body weight in the 24h following the injection.
  •  Oral administration of OEA confirmed that OEA acts peripherally. A significant decrease of food intake on 24h was observed at 200 mg/kg of oral OEA.
  • In another study, it has been shown that OEA influence the synthesis of  satiety signaling biomarkers, such as glucagon-like peptide-1, chlecystokinin and peptide YY which have satietogenic effects and ghrelin, which stimulated appetite.
  • Satietogenic properties of OEA can also be partially explained by its action on the gastrointestinal tract itself. Indeed, OEA delays gastric emptying and slows down intestinal motility. The delay of these parameters has a strong influence on nutrient absorption and thus on food intake control
  •   OEA showed agonist properties on  transient receptor potential vanilloid type 1 (TRPV 1) by stopping Ca2+ uptake in cells expressing TRPV1. The mechanism of action on OEA on TRPV1is linked to a Ca2+ concentration modulation inside the cell, inducing an effect on vagal sensory nerves and, consequently on food intake regulation.


Oleoylethanolamide and lipid metabolism

  • A decrease in body weight is not only due satietogenic effect but also due to direct effect on lipid metabolism.
  • OEA also lowers the blood plasma cholesterol levels in wild type mice.
  • OEA has lipolytic properties through

    Increase in lipolysis
    Intraperitoneal administration of 5mg/kg body weight in rats increased the expression of FAT/CD36 fatty acid translocase) in adipose tissue. This increased the amount of free fatty acids suggesting an increase in lipolysis.

    Inhibition of adipogensis in adipose tissue
    OEA acts and agonist for transient receptor potential vanilloid type 1 (TRPV 1) that is expressed in preadipocyte. Once activated, this receptor inhibits differentiation of preadipocyte and thus adipogensis is inhibited

       

         Activation of β oxidation in muscle
       OEA regulates peroxisome proliferator-activated receptor alpha (PPAR-α) in fatty acid β oxidation in muscle.


Image:  http://www.earthtimes.org/newsimage/skinny-worms-provide-approach-o...

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