Administration of URB597, Oleoylethanolamide or Palmitoylethanolamide Increases Waking and Dopamine in Rats

Murillo-Rodrı́guez, Eric; Palomero-Rivero, Marcela; Millán-Aldaco, Diana; Arias-Carrión, Óscar; Drucker-Colı́n, René

doi:10.1371/journal.pone.0020766

Cited by 42 publications

(44 citation statements)

References 36 publications

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“…Moreover, in another experiment conducted by Murillo‐Rodríguez and colleagues in rats , local administration of the FAAH inhibitor URB597, which increases the levels of OEA in the brain and OEA in the lateral hypothalamus and the dorsal raphe nuclei showed increased levels of dopamine in nucleus accumbens shell (NAcS). Subsequent investigations in the rat midbrain demonstrated a modulation of dopaminergic function due to the peculiar capability of OEA to regulate nicotinic receptors containing β2 subunits, a nicotinic acetylcholine receptor symbolized as β2*‐nAChRs expressed by dopamine neurons that enhance the reward system from a brain stimulus .…”

Section: The Gut Lipid Messenger Oleoylethanolamide Recruits the Foodmentioning

confidence: 99%

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

Sihag

Jones

2017

Obesity Reviews

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Fatty acid ethanolamides are lipid mediators that regulate a plethora of physiological functions. One such bioactive lipid mediator, oleoylethanolamide (OEA), is a potent agonist of the peroxisome proliferator-activated receptor-alpha (PPAR-α), which modulates increased expression of the fatty acid translocase CD36 that enables the regulation of feeding behaviour. Consumption of dietary fat rich in oleic acid activates taste receptors in the gut activating specific enzymes that lead to the formation of OEA. OEA further combines with PPAR-α to enable fat oxidation in the liver, resulting in enhanced energy production. Evidence suggests that sustained ingestion of a high-fat diet abolishes the anorexic signal of OEA. Additionally, malfunction of the enterocyte that transforms oleic acid produced during fat digestion into OEA might be responsible for reduced satiety and hyperphagia, resulting in overweight and obesity. Thus, OEA anorectic signalling may be an essential element of the physiology and metabolic system regulating dietary fat intake and obesity. The evidence reviewed in this article 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.

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Section: The Gut Lipid Messenger Oleoylethanolamide Recruits the Foodmentioning

confidence: 99%

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

Sihag

Jones

2017

Obesity Reviews

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“…[1] On the other hand, the use of proteins that are abundant in,for example, green alga Chlorella sp. [4][5][6][7][8][9][10][11][12][13][14][15] Paltmitoyl ethanol amide (PAE) was already recognized as an anti-inflammatory agent five decades ago. [1] Them ain components in proteins are amino acids, which can be catalytically hydrogenated to give the corresponding amino alcohols.…”

Section: Introductionmentioning

confidence: 99%

“…[2] The latter react with acids to form alkylamides, which are used in various applications, such as surfactants [3] and pharmaceuticals. [8] Apart from various diseases in which PAEh as been reported as ap otentiald rug, such as psoriasis, [9] angina, [10] migraine, [11] Alzheimer's disease, [12] Parkinson's disease, [13] and cancer, [14] N-acylamides have also been used as surfactants and in cosmetics. [4] Later on, PAEw as used in several pharmaceuticals, as summarized in Refs.…”

Section: Introductionmentioning

confidence: 99%

“…[2] The latter react with acids to form alkylamides, which are used in various applications, such as surfactants [3] and pharmaceuticals. [4][5][6][7][8][9][10][11][12][13][14][15] Paltmitoyl ethanol amide (PAE) was already recognized as an anti-inflammatory agent five decades ago. [4] Later on, PAEw as used in several pharmaceuticals, as summarized in Refs.…”

Section: Introductionmentioning

confidence: 99%

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Pharmaceuticals and Surfactants from Alga‐Derived Feedstock: Amidation of Fatty Acids and Their Derivatives with Amino Alcohols

et al. 2015

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Amidation of renewable feedstocks, such as fatty acids, esters, and Chlorella alga based biodiesel, was demonstrated with zeolites and mesoporous materials as catalysts and ethanolamine, alaninol, and leucinol. The last two can be derived from amino acids present in alga. The main products were fatty alkanol amides and the corresponding ester amines, as confirmed by NMR and IR spectroscopy. Thermal amidation of technical-grade oleic acid and stearic acid at 180 °C with ethanolamine were non-negligible; both gave 61% conversion. In the amidation of stearic acid with ethanolamine, the conversion over H-Beta-150 was 80% after 3 h, whereas only 63% conversion was achieved for oleic acid; this shows that a microporous catalyst is not suitable for this acid and exhibits a wrinkled conformation. The highest selectivity to stearoyl ethanolamide of 92% was achieved with mildly acidic H-MCM-41 at 70% conversion in 3 h at 180 °C. Highly acidic catalysts favored the formation of the ester amine, whereas the amide was obtained with a catalyst that exhibited an optimum acidity. The conversion levels achieved with different fatty acids in the range C12-C18 were similar; this shows that the fatty acid length does not affect the amidation rate. The amidation of methyl palmitate and biodiesel gave low conversions over an acidic catalyst, which suggested that the reaction mechanism in the amidation of esters was different.

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“…The activity of FAAH has been studied using highly selective inhibitors [13,14], including URB597 [3,5,6,15-17]. …”

Section: Introductionmentioning

confidence: 99%

Cellular viability effects of fatty acid amide hydrolase inhibition on cerebellar neurons

Lueneberg¹,

Domínguez²,

Arias-Carrión³

et al. 2011

Int Arch Med

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The endocannabinoid anandamide (ANA) participates in the control of cell death inducing the formation of apoptotic bodies and DNA fragmentation. The aim of this study was to evaluate whether the ANA degrading enzyme, the fatty acid amide hydrolase (FAAH), would induce cellular death. Experiments were performed in cerebellar granule neurons cultured with the FAAH inhibitor, URB597 (25, 50 or 100 nM) as well as endogenous lipids such as oleoylethanolamide (OEA) or palmitoylethanolamide (PEA) and cellular viability was determined by MTT test. Neurons cultured with URB597 (25, 50 or 100 nM) displayed a decrease in cellular viability. In addition, if cultured with OEA (25 nM) or PEA (100 nM), cellular death was found. These results further suggest that URB597, OEA or PEA promote cellular death.

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Administration of URB597, Oleoylethanolamide or Palmitoylethanolamide Increases Waking and Dopamine in Rats

Cited by 42 publications

References 36 publications

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

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

Pharmaceuticals and Surfactants from Alga‐Derived Feedstock: Amidation of Fatty Acids and Their Derivatives with Amino Alcohols

Cellular viability effects of fatty acid amide hydrolase inhibition on cerebellar neurons

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