Oleoylethanolamide (OEA) is synthesized and mobilized in the proximal small intestine from diet-derived oleic acid, such as olive oils. High-fat diet can inhibit OEA production in the intestine. OEA reduces food intake by activating homeostatic oxytocin and histamine brain circuitry as well as hedonic dopamine pathways. There is evidence that OEA may also attenuate hedonic cannabinoid receptor 1 (CB1R) signaling, the activation of which is associated with increased food intake. OEA reduces lipid transport into adipocytes to decrease fat mass. Further elucidation of the effects of OEA on food intake and lipid metabolism will aid in the determination of physiological mechanisms that can be targeted to develop more effective obesity therapies.To get more news about Oleoylethanolamide(OEA)[/url], cofttek official website is the best place for you.
Oleoylethanolamide (OEA) is an agonist of peroxisome proliferator-activated receptor-α (PPAR-α). N-Oleoylethanolamide generates an intestinal signal that stimulates central dopamine activity establishing a link between caloric-homeostatic and hedonic-homeostatic controllers. Oleoylethanolamide has been implicated as the molecular mechanism associated with gastric bypass success. N-Oleoylethanolamide is a selective GPR55 agonist.