Oleoylethanolamide---Control the food intake

 

  1. Regulation of OEA levels

 

In primary cultures of rat brain neurons, the synthesis of OEA and its precursor NAPE is stimulated by a variety of pharmacological treatments that elevate intracellular calcium levels. These include membrane-depolarizingagents such as kainate (a glutamate receptor agonist) andcalcium ionophores such as ionomycin. Inaddition, OEA formation may be elicited in cortical neu-rons by coactivation of N-methyl-D-aspartate (NMDA)-type glutamate receptors and cholinergic muscarinic receptors. However, the physiological stimuli thatcontrol brain OEA levels in live animals remain unex-plored.In the duodenum and jejunum of rats and mice, OEA levels change in response to nutrient status: they arelower in food-deprived than free-feeding animals, andreturn to baseline values upon refeeding. These alterations are restricted to the upper intestine a structureintimately involved in the control of feeding behavior and are accompanied by parallel changes in NATactivity within the upper region of the intestine, whichis suggestive of a stimulatory effect of feeding on OEAsynthesis . OEA levels in the rodent small intestine also display diurnal fluctuations. They are higher during the daytime,when animals are satiated, and lower during the night,when they are awake and actively feeding. A paralleldiurnal cycle is present in rat white adipose tissue, but notin the liver. The molecular mechanisms that control OEA turnover in response to feeding and diurnalcycles have not been characterized.

 

  1. OEA regulates feeding behavior

 

The finding that intestinal OEA levels are elevated in thepost-absorptive state suggests that this lipid amide maycontribute to the regulation of feeding behavior. In supportof this possibility, administration of OEA to rats or micewas found to produce a dose and time-dependent inhibitionof food intake. This effect is bothstructurally and behaviorally selective: close structuralanalogues of OEA are either less potent than OEA at reducing feeding (e.g. PEA) or are completely ineffective(e.g. anandamide or oleic acid). In fact, anandamidestimulates feeding in partially satiated animals via activa-tion of cannabinoid receptors located both in the brainand peripheral tissues. Importantly, OEA is inac-tive in a rat model of conditioned taste aversion, does notcause anxiety-like behaviors in the elevated plus-mazetest and does not change plasma corticosterone levels, indicating that its anorexiant effects cannot be accountedfor by malaise anxiety or stress. As discussedlater, the ability of OEA to reduce feeding may be predominantly, if not exclusively, ascribed to an enhancedstate of satiety. At doses higher than those required to produce hypophagia, OEA causes moderate hypolocomotion. This effect is unlikely to contribute to the anorexiant properties of OEA, however, not only for its cleardose separation, but also because OEA has no effect on water intake or need-induced sodium appetite.

 

  1. OEA is an endogenous PPAR-aaagonist

 

OEA is an endogenous PPAR-aaagonistAlthough the structural and behavioral specificity ofOEA and other FAEs suggest that these biomoleculesmay interact with a selective receptor site, the identity of this putative receptor has long remained elusive. The fact that OEA resembles lipid compoundsthat activate the PPAR family of nuclear receptors, suchas non-esterified fatty acids, prompted us to explorethe possibility that this molecule might target one of theseligand-activated transcription factors. PPAR receptors, first identified in 1992, are a family of ligand-activated transcription factors that comprisesthree known isoforms, PPAR-a, PPAR-d(also called PPAR-b) and PPAR-g. PPAR-areceptors, the moleculartarget of the fibrate class of antihyperlipidemic drugs, induce a variety of transcriptional changes that result inincreased fatty-acid catabolism, reduced blood lipid levelsand lowered body-weight gain.They also regulate inflammation through transcriptionaland non-transcriptional actions.

 

Like PPAR-a, PPAR-dstimulates adipose tissue utilization and protectsanimals from diet-induced obesity. In addition, activation of this receptor modulates muscle function by enhancing the transformation of type II to type I fibersand stimulating mitochondrial biogenesis. In contrastto PPAR-aand PPAR-d, PPAR-gactivation facilitates fatstorage, promotes adipocyte maturation and improves insulin sensitivity. These results indicatethat OEA is a high-affinity agonist of PPAR-a. Does PPAR-aactivation contribute to the hypophagic actions of OEA? Experiments in genetically modifiedmice show that OEA does not reduce feeding in animalslacking a functional PPAR-agene. Underscoringthe selectivity of this defect, PPAR-a-deficient mice retain the ability to respond to other appetite suppressants,such as d-fenfluramine and cholecystokinin. The possibility that OEA causes hypophagia by activating PPAR-ais supported by two additional findings.

 

  1. The raw material supplier of Oleoylethanolamide (OEA)

One can purchase an OEA drug from a reputed and proficient drug store located nearby your dwelling place or can even buy it by ordering online. But one has to be very alert in this respect as all the suppliers of this drug might not be genuine.

So, always check the reputation and the proficiency of the online drug stores and for that, it is always advisable to go through the details of the reviews of the experienced purchasers. Be sure about the packaging of the product like whether it is properly sealed or not to avoid any type of contamination which can result in some dangerous issues in the health front.

  1. Oleoylethanolamide (oea) in the form of powder

OEA in its original state is not found in the form of tablets or capsules. However, you can buy OEA powder in bulkin the market if required.  This powder form is incorporated in the finished product by regularizing it to 15 % OEA or 50 % OEA oleic acid. The blueprint of Cima OEA is maintained between 90 % to 95 % especially among the purchasers of Europe and the United States.

 

  1. Buy Oleoylethanolamide (OEA) powder in bulk

 

You can place an online order for bulk purchase of powder or can even buy from reputed local stores. Storage is pretty simple in the case of OEA powder. You need to store it at room temperature. But, it should not come in contact with the moisture or direct sun rays. So, you need to keep it tightly sealed in a cool and dry place.

 

  1. STABILITY

 

Uses of OEAcan help you in many ways! For this reason, highly recommendable to everyone as it has no side effects. It can even induce a healthy lifestyle within your family making all of you grow and glow in shape, style, and with esteem and confidence. Keeping and maintaining your body in shape, especially for those who are a little bit obese, will not only make you feel happy but will also make others feel happy and proud too about you.

 

OEA will also help you to release out mental stress helping you to create a positive impression in others’ minds. Thus, instead of feeling upset and unhappy, it is high time to take an action and start using OEA and you will be extremely amazed to see its magical powers and you will feel healed and caressed.

References

 

  1. Stella N. and Piomelli D. (2001) Receptor-dependent formationof endogenous cannabinoids in cortical neurons. Eur. J. Phar-macol. 425:189–19625

 

  1. Rodríguez de Fonseca F., Navarro M., Gómez R., Escuredo L.,Nava F., Fu J. et al. (2001) An anorexic lipid mediator regulatedby feeding. Nature 414:209–21226

 

  1. Ritter R. C. (2004) Gastrointestinal mechanisms of satiation forfood. Physiol. Behav. 81:249–27327

 

  1. Fu J., Gaetani S., Oveisi F., Lo Verme J., Serrano A., Rodriguezde Fonseca F. et al. (2003) Oleylethanolamide regulates feedingand body weight through activation of the nuclear receptorPPAR-alpha. Nature 425:90–9328

 

  1. Oveisi F., Gaetani S., Eng K. T. and Piomelli D. (2004)Oleoylethanolamide inhibits food intake in free-feeding rats after oral administration. Pharmacol. Res. 49:461–46629

 

  1. Nielsen M. J., Petersen G., Astrup A. and Hansen H. S. (2004)Food intake is inhibited by oral oleoylethanolamide. J. Lipid.Res. 45:1027–102930

 

  1. McKay B. M. and Ritter R. C. (2004) Oleoylethanolamide induces rapid reduction of short-term food intake in intact andvagotomized rats. Program No. 427.12, Society for Neuro-science, Washington, DC, online