Role of oleoylethanolamide as a feeding regulator in goldfish

Abstract

Oleoylethanolamide (OEA) is a bioactive lipid mediator, produced in the intestine and other tissues, which is involved in energy balance regulation in mammals, modulating feeding and lipid metabolism. The purpose of the present study was to investigate the presence and possible role of OEA in feeding regulation in goldfish (Carassius auratus). We assessed whether goldfish peripheral tissues and brain contain OEA and their regulation by nutritional status. OEA was detected in all studied tissues (liver, intestinal bulb, proximal intestine, muscle, hypothalamus, telencephalon and brainstem). Food deprivation (48 h) reduced intestinal OEA levels and levels increased upon re-feeding, suggesting that this compound may be involved in the short-term regulation of food intake in goldfish, as a satiety factor. Next, the effects of acute intraperitoneal administration of OEA on feeding, swimming and plasma levels of glucose and triglycerides were analysed. Food intake, swimming activity and circulating triglyceride levels were reduced by OEA 2 h post-injection. Finally, the possible interplay among OEA and other feeding regulators (leptin, cholecystokinin, ghrelin, neuropeptide Y, orexin and monoamines) was investigated. OEA actions on energy homeostasis in goldfish could be mediated, at least in part, through interactions with ghrelin and the serotonergic system, as OEA treatment reduced ghrelin expression in the intestinal bulb, and increased serotonergic activity in the telencephalon. In summary, our results indicate for the first time in fish that OEA could be involved in the regulation of feeding, swimming and lipid metabolism, suggesting a high conservation of OEA actions in energy balance throughout vertebrate evolution.

The effects of oleoylethanolamide, an endogenous PPAR‐α agonist, on risk factors for NAFLD: A systematic review

“…significantly reduced both serum levels of TG and cholesterol without having any effect on HDL‐C and glucose levels . Levels of serum TG, but not glucose, were also reduced via OEA treatment (5 μg/g body weight) in goldfish, indicating the protective effects of OEA on TG levels in vertebrates . Fu et al reported increased PPAR‐α gene expression and other PPAR‐α target genes, including liver fatty‐acid binding protein (L‐FABP), uncoupling protein 2 )UCP‐2(, and FAT/CD36 after OEA administration (5 mg/kg, i.p.).…”

“…OEA plays a pivotal role in lipid metabolism by modulating lipids in circulation and tissues in addition to its satietogenic effect . Several experimental studies have shown the useful effects of OEA on lipid profiles (Supplemental Table 1) . Further investigations have indicated that the lipolytic activity of OEA and its effects on fatty acid mobilization by activating PPAR‐α and PPAR‐α target genes contribute to lipid metabolism .…”

Mast Cell-Derived Histamine Regulates Liver Ketogenesis via Oleoylethanolamide Signaling

“…Third, viral-mediated enhancement of OEA production in rat jejunum reduces food intake and concomitantly increases local expression of PPAR-a target genes (Fu et al, 2008). Finally, OEA levels in small intestine from various vertebrate species, including fish, snakes, and rodents, rise from %50 nM in the fasting state to R250 nM after feeding (Astarita et al, 2006b;Fu et al, 2007;Tinoco et al, 2014;Igarashi et al, 2017), a concentration range that is compatible with PPAR-a activation (Fu et al, 2003;Astarita et al, 2006a). In sum, the available data indicate that OEA is a physiologically relevant endogenous agonist for small-intestinal PPAR-a, which participates in the control of satiety .…”

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

“…Overall, from the cumulative evidence in humans and rodents and work done by Tinoco and colleagues , it is worth noting that a strong association between OEA and other feeding regulators exists imparting the satiating/anorexic properties. Therefore, future studies are required to clarify the satiating efficacy of OEA alone by performing studies using knock‐out animal models for specific receptors involved in inducing satiation.…”