The Fat-Induced Satiety Factor Oleoylethanolamide Suppresses Feeding through Central Release of Oxytocin

Gaetani, Silvana; Fu, Jin; Cassano, Tommaso; Dipasquale, Pasqua; Romano, Adele; Righetti, Laura; Cianci, Silvia; Laconca, Leonardo; Giannini, Elisa; Scaccianoce, Sergio; Mairesse, Jérôme; Cuomo, V.; Piomelli, Daniele

doi:10.1523/jneurosci.0036-10.2010

Cited by 104 publications

(134 citation statements)

References 38 publications

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“…A previous study in rats (Serrano et al, 2011) demonstrated that OEA failed to modulate hypothalamic expression of NPY and AgRP (agouti-related protein) in experimental conditions (fed and 24 h fasted) similar to those of the present study. These data support the hypothesis that these orexigenic peptides in hypothalamus do not play a critical role in the anorectic effect of OEA in fish and mammals, although interactions between OEA and other orexigenic and anorexigenic neuropeptides, such as CART and oxytocin (Serrano et al, 2011;Gaetani et al, 2010), cannot be ruled out.…”

Section: Interplay Between Oea and Other Feeding Regulatorssupporting

confidence: 80%

“…Anorectic actions of OEA can be mediated through the modulation of central and peripheral signals involved in feeding regulation. It has been described that this FAE suppresses feeding by activating hypothalamic oxytocin transmission (Gaetani et al, 2010;Romano et al, 2013). Moreover, interactions between OEA and hypothalamic monoamines and cocaine-and amphetamineregulated transcript (CART) have also been suggested (Serrano et al, 2011).…”

Section: Introductionmentioning

confidence: 98%

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Role of oleoylethanolamide as a feeding regulator in goldfish

Tinoco

Armirotti

Isorna

et al. 2014

Journal of Experimental Biology

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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.

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Section: Interplay Between Oea and Other Feeding Regulatorssupporting

confidence: 80%

Section: Introductionmentioning

confidence: 98%

Role of oleoylethanolamide as a feeding regulator in goldfish

Tinoco

Armirotti

Isorna

et al. 2014

Journal of Experimental Biology

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“…OEA is synthesized in several peripheral tissues and in the CNS (22) and in mammals it has been described as a mediator of numerous metabolic processes (4). OEA secreted by enterocytes serves as a fatsensing molecule that signals to satiety centers in the brain by engaging vagus nerve sensory fibers (2,4,23) and suppresses feeding by indirectly activating central oxytocin transmission in the PVN and SON (3). However, it is not known if other neurotransmitter systems integrate the peripheral signaling of OEA with effector hypothalamic nuclei.…”

Section: Discussionmentioning

confidence: 99%

“…The fatty acid amide oleoylethanolamide (OEA) is released by the small intestine in a stimulus-dependent manner and suppresses food intake by activating peroxisome proliferator-activated receptor-α (PPAR-α) (1). Systemic administration of OEA induces c-Fos mRNA expression through the vagus nerve to the nucleus of the solitary tract (NST), supraoptic nuclei (SON), and paraventricular hypothalamic nuclei (PVN) and increases the expression of oxytocin (2,3), which is involved in the central coordination of homeostatic signals and feeding behavior (4). However, it is not known whether OEA recruits other neurotransmitter systems in the brain to reduce food intake.…”

mentioning

confidence: 99%

Satiety factor oleoylethanolamide recruits the brain histaminergic system to inhibit food intake

Provensi

Coccurello

Umehara

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

108

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Key factors driving eating behavior are hunger and satiety, which are controlled by a complex interplay of central neurotransmitter systems and peripheral stimuli. The lipid-derived messenger oleoylethanolamide (OEA) is released by enterocytes in response to fat intake and indirectly signals satiety to hypothalamic nuclei. Brain histamine is released during the appetitive phase to provide a high level of arousal in anticipation of feeding, and mediates satiety. However, despite the possible functional overlap of satiety signals, it is not known whether histamine participates in OEA-induced hypophagia. Using different experimental settings and diets, we report that the anorexiant effect of OEA is significantly attenuated in mice deficient in the histamine-synthesizing enzyme histidine decarboxylase (HDC-KO) or acutely depleted of histamine via interocerebroventricular infusion of the HDC blocker α-fluoromethylhistidine (α-FMH). α-FMH abolished OEA-induced early occurrence of satiety onset while increasing histamine release in the CNS with an H 3 receptor antagonist-increased hypophagia. OEA augmented histamine release in the cortex of fasted mice within a time window compatible to its anorexic effects. OEA also increased c-Fos expression in the oxytocin neurons of the paraventricular nuclei of WT but not HDC-KO mice. The density of c-Fos immunoreactive neurons in other brain regions that receive histaminergic innervation and participate in the expression of feeding behavior was comparable in OEA-treated WT and HDC-KO mice. Our results demonstrate that OEA requires the integrity of the brain histamine system to fully exert its hypophagic effect and that the oxytocin neuron-rich nuclei are the likely hypothalamic area where brain histamine influences the central effects of OEA.histamine receptors | behavioral satiety sequence | BSS | paraventricular hypothalamic nuclei | PVN E ating behavior is regulated by central neurotransmitter systems and peripheral stimuli that interact to change the behavioral state and concur to alter homeostatic aspects of appetite and energy expenditure. The fatty acid amide oleoylethanolamide (OEA) is released by the small intestine in a stimulus-dependent manner and suppresses food intake by activating peroxisome proliferator-activated receptor-α (PPAR-α) (1). Systemic administration of OEA induces c-Fos mRNA expression through the vagus nerve to the nucleus of the solitary tract (NST), supraoptic nuclei (SON), and paraventricular hypothalamic nuclei (PVN) and increases the expression of oxytocin (2, 3), which is involved in the central coordination of homeostatic signals and feeding behavior (4). However, it is not known whether OEA recruits other neurotransmitter systems in the brain to reduce food intake. Histaminergic neurons are clustered in the hypothalamic tuberomammillary nuclei (TMN). They send projections organized in functionally distinct circuits impinging on different brain regions (5), and their firing frequency changes according to the behavioral state (6). Brain histamin...

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“…Sun et al 13 Romano and Lograno 14 nd 2-AG nd Kozak et al 15 nd nd OEA Fu et al 16 and Sun et al 13 Fu et al 16 and Sun et al 13 Melis et al 17 and Zhou et al 18 Fu et al, 16 Guzman et al, 19 Sun et al, 13 Campolongo et al, 20 and Gaetani et al 21 PEA nd Lo Verme et al 22 Melis et al, 17 Koch et al, 23 Scuderi et al, 24 Scuderi et al, 25 Romano and Lograno, 14 and de Novellis et al 26 Lo Verme et al, 22 Lo Verme et al, 27 Di Paola et al, 28 D'Agostino et al, 29 and Sasso et al 30 Noladin ether Sun et al 13 Sun et al 13 nd nd Virodhamine Sun et al 13 Sun et al 13 nd nd…”

Section: P Eroxisomementioning

confidence: 99%

Cannabinoid activation of peroxisome proliferator‐activated receptors: an update and review of the physiological relevance

O’Sullivan

2012

WIREs Membr Transp Signal

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Since 2002, evidence has been building that cannabinoids, including endocannabinoids and endocannabinoid-like compounds, phytocannabinoids and synthetic cannabinoid ligands, bind to and activate the different isoforms of the nuclear receptors, peroxisome proliferator-activated receptors (PPARs; α, β, and γ ). This has been shown through the use of reporter gene assays, binding studies, the use of antagonists and knockout animals. Increasing use of tools to assess a potential role for PPAR activation in underpinning the physiological effects of cannabinoids means that a picture is emerging of the relevance of PPAR activation by cannabinoids. There is now evidence that activation of PPARα and γ mediate some of the anti-inflammatory, analgesic, neuroprotective, and cardiovascular effects of cannabinoids, sometimes in combination with activation of the more traditional target sites of action such as CB 1 , CB 2 , and TRPV1. There is also a role for PPARα activation by cannabinoids in some of their central effects including memory acquisition, reward processing, food intake and body weight regulation. Activation of PPARγ plays a role in the apoptotic effects of cannabinoids. However, much further work is required to fully establish the profile of cannabinoid compounds at all isoforms of the PPAR family and the relevance of this in normal physiology and pathological situations.

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The Fat-Induced Satiety Factor Oleoylethanolamide Suppresses Feeding through Central Release of Oxytocin

Cited by 104 publications

References 38 publications

Role of oleoylethanolamide as a feeding regulator in goldfish

Role of oleoylethanolamide as a feeding regulator in goldfish

Satiety factor oleoylethanolamide recruits the brain histaminergic system to inhibit food intake

Cannabinoid activation of peroxisome proliferator‐activated receptors: an update and review of the physiological relevance

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