Regulation of food intake by oleoylethanolamide

  title={Regulation of food intake by oleoylethanolamide},
  author={Jesse Lo Verme and Silvana Gaetani and J. Fu and Fariba Oveisi and K. Burton and Daniele Piomelli},
  journal={Cellular and Molecular Life Sciences},
Abstract.Oleoylethanolamide (OEA), the naturally occurring amide of ethanolamine and oleic acid, is an endogenous lipid that modulates feeding, body weight and lipid metabolism by binding with high affinity to the ligand-activated transcription factor, peroxisome proliferator-activated receptor-alpha (PPAR-α). In the present article, we describe the biochemical pathways responsible for the initiation and termination of OEA signaling, and outline the pharmacological properties of this compound… 

Feeding regulation by oleoylethanolamide synthesized from dietary oleic acid.

Oleoyl‐ethanolamide (OEA): A bioactive lipid derived from oleic acid and phosphatidylethanol‐amine

In rodents, intraperitoneal administration of OEA induces satiety and peripheral utilization of lipid substrate, and the proximal intestine seems to be a target organ for satiety control.

eview ole of anorectic N-acylethanolamines in intestinal physiology and atiety control with respect to dietary fat arald

Anandamide is a well-known agonist for the cannabinoid receptors. Along with endogenous anandamide other non-endocannabinoid N-acylethanolamines are also formed, apparently in higher amounts. These

N-acylethanolamines, anandamide and food intake.

Oleoylethanolamide: The role of a bioactive lipid amide in modulating eating behaviour

  • J. SihagP. J. Jones
  • Biology
    Obesity reviews : an official journal of the International Association for the Study of Obesity
  • 2018
Evidence indicates that intake of oleic acid, and thereby the resulting OEA imparting anorexic properties, is dependent on CD36, PPAR‐α, enterocyte fat sensory receptors, histamine, oxytocin and dopamine; leading to increased fat oxidation and enhanced energy expenditure to induce satiety and increase feeding latency; and that a disruption in any of these systems will cease/curb fat‐induced satiety.

Brain molecules and appetite: the case of oleoylethanolamide.

The emerging molecular mechanism of anorexia induced by OEA is highlighted, which has been suggested that the ingestion of dietary fat stimulates epithelial cells of the small intestine and promotes the synthesis and release of OEA.

Food Intake Regulates Oleoylethanolamide Formation and Degradation in the Proximal Small Intestine*

It is shown that feeding stimulates OEA mobilization in the mucosal layer of rat duodenum and jejunum but not in the serosal layer from the same intestinal segments in other sections of the gastrointestinal tract or in a broad series of internal organs and tissues.

Cold Exposure Stimulates Synthesis of the Bioactive Lipid Oleoylethanolamide in Rat Adipose Tissue*

It is shown that cold exposure increases OEA levels in rat white adipose tissue but not in liver or intestine, and a role for the sympathetic nervous system in regulating OEA biosynthesis is suggested.

Pharmacological Characterization of Hydrolysis-Resistant Analogs of Oleoylethanolamide with Potent Anorexiant Properties

Oleoylethanolamide analogs that resist enzymatic hydrolysis, activate PPAR-α with high potency in vitro, and persistently reduce feeding when administered in vivo either parenterally or orally are described.



An anorexic lipid mediator regulated by feeding

It is shown that, in rats, food deprivation markedly reduces OEA biosynthesis in the small intestine, and results indicate that OEA is a lipid mediator involved in the peripheral regulation of feeding.

Oleylethanolamide regulates feeding and body weight through activation of the nuclear receptor PPAR-α

The results, which show that OEA induces satiety by activating PPAR-α, identify an unexpected role for this nuclear receptor in regulating behaviour, and raise possibilities for the treatment of eating disorders, are identified.

Modulation of Meal Pattern in the Rat by the Anorexic Lipid Mediator Oleoylethanolamide

The results suggest that OEA may participate in the regulation of satiety and may provide a chemical scaffold for the design of novel appetite-suppressing medications.

Oleoylethanolamide stimulates lipolysis by activating the nuclear receptor peroxisome proliferator-activated receptor alpha (PPAR-alpha).

The results suggest that OEA stimulates fat utilization through activation of PPAR-alpha and that this effect may contribute to its anti-obesity actions.

Pharmacological activity of fatty acid amides is regulated, but not mediated, by fatty acid amide hydrolase in vivo.

The results indicate that FAAH is a key regulator, but not mediator of FAA activity in vivo, and suggest that FAAs represent a family of signaling lipids that, despite sharing similar chemical structures and a common pathway for catabolism, produce their behavioral effects through distinct receptor systems in vivo.

The N-acylation-phosphodiesterase pathway and cell signalling.

Hypolipidemic drugs, polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome proliferator-activated receptors alpha and delta.

It is shown here that specific FAs, eicosanoids, and hypolipidemic drugs are ligands for PPARalpha or PPARdelta, and a novel conformation-based assay is developed that screens activators for their ability to bind to PPAR alpha/delta and induce DNA binding.

Hypolipidemic drugs, polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome proliferator-activated receptors α and δ

It is shown here that specific FAs, eicosanoids, and hypolipidemic drugs are ligands for PPARα or PPARδ, and a novel conformation-based assay is developed that screens activators for their ability to bind to PPAR α/δ and induce DNA binding.

Stearoylethanolamide exerts anorexic effects in mice via downregulation of liver stearoyl‐coenzyme A desaturase‐1 mRNA expression

  • S. TerrazzinoFiorenzo Berto A. Leon
  • Biology, Chemistry
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2004
The novel observation provided here that SEA reduces food intake in mice in a structurally selective manner, in turn, correlated with downregulation of liver SCD‐1 mRNA expression, has the potential of providing new insights on a class of lipid mediators with suitable properties for the pharmacological treatment of over‐eating dysfunctions.