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Bioactive Lipid Mediator-oleoylethanolamide (OEA)

What is Oleoylethanolamide (OEA) ? Oleoylethanolamine (OEA) is an endogenous peroxisome proliferator-activated receptor alpha (PPAR-α) agonist. It is a naturally occurring ethanolamide lipid that regulates feeding and body weight in vertebrates ranging from mice to pythons. It has been described...

What is Oleoylethanolamide (OEA) ?

Oleoylethanolamine (OEA) is an endogenous peroxisome proliferator-activated receptor alpha (PPAR-α) agonist. It is a naturally occurring ethanolamide lipid that regulates feeding and body weight in vertebrates ranging from mice to pythons.

It has been described as a peripherally agent that reducing food intake and fat burner.


Product details: 

Product name: Oleoylethanolamide, N-Oleoylethanolamide, OEA

CAS No: 111-58-0

Assay: 85%, 95%

Molecular Formular: C20H39NO2

Molecular Weight:325.5

Test Method: GC

Appearance :white to light yellow powder

 

The key benefits of OEA include:

Function as an appetite suppressant, fat burner, lower cholesterol levels, etc.

 

Application:

Used as dietary supplement;

Many end products has made it as a part of an weight loss and fat burner ingredients.

 

Sources of Oleoylethanolamide (OEA)

There are two sources of getting Oleoylethanolamide (OEA), one is from natural plants, and the other is by purely synthesized in the lab.
Achyranthes Aspera, native to India, China and many other Asian countries, is said to contain Oleoylethanolamide OEA. The problem of the natural-sourced Oleoylethanolamide is that there is only ratio extract is available, 15:1 is a popular spec, and it is not as potent as the clients or supplement manufacturers expect. Of course, it can be higher, but the cost will be extremely high, thus it is not so practical to manufacture natural Oleoylethanolamide OEA in bulk.

The mainstream source of Oleoylethanolamide is synthesized from oleic acid, served as a precursor of OEA, which is then cleaved by N-acyl-phosphatidylethanolamine-selective phospholipase D (PLD) to release Oleoylethanolamide OEA.

 

Mechanism :

Current data shows that oleoylethanolamide OEA induces satiety. How does this happen? What might be the mechanism of action of OEA on feeding suppression? It has been suggested that the anorexic effect caused by OEA requires intact sensory vagal fibers as well as an activation of the nucleus of the solitary tract in the brainstem and the paraventricular nucleus in the hypothalamus. In this regard, animals with lesion in the peripheral sensory fibers failed to respond to the pharmacological administrations of OEA whereas surgical resection of the sympathetic celiac-superior mesenteric ganglion complex bocks feeding-induced OEA production in rat small-intestinal cells.

Additionally, it has been suggested that the food-intake suppression actions of OEA are mediated by the peroxisome proliferator-activated receptor-α(PPAR-α), a nuclear receptor linked to the regulation of absorption, storage and utilization of dietary fat. Regarding this, the hypophagic effects of OEA are abolished in PPAR-α-null mice whereas food suppression is mimicked by PPAR-αagonists.

Overall, the above data suggest that OEA could be mediating anorexia via action of PPAR-αreceptors. However, further studies are needed to elucidate the mechanisms of action of PPAR-α in feeding.
The main role of oleoylethanolamide is to serve as a fat sensor, controlling fat intake and helping the metabolic network to adapt to the dietary fat load.

 

OEA: A Novel Potential Pharmacological Alternative to Cannabinoid Antagonists for the Control of Appetite 

The initial pharmaceutical interest for the endocannabinoid system as a target for antiobesity therapies has been restricted by the severe adverse effects of the CB1 antagonist rimonabant. This study points at oleoylethanolamide (OEA), a monounsaturated analogue, and functional antagonist of anandamide, as a potential and safer antiobesity alternative to CB1 antagonism. Mice treated with equal doses (5 or 10 mg/kg, i.p.) of OEA or rimonabant were analyzed for the progressive expression of spontaneous behaviors (eating, grooming, rearing, locomotion, and resting) occurring during the development of satiety, according to the paradigm called behavioral satiety sequence (BSS). Both drugs reduced food (wet mash) intake to a similar extent. OEA treatment decreased eating activity within the first 30 min and caused a temporary increase of resting time that was not accompanied by any decline of horizontal, vertical and total motor activity. Besides decreasing eating activity, rimonabant caused a marked increase of the time spent grooming and decreased horizontal motor activity, alterations that might be indicative of aversive nonmotivational effects on feeding. These results support the idea that OEA suppresses appetite by stimulating satiety and that its profile of action might be predictive of safer effects in humans as a novel antiobesity treatment.


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