An anorexic lipid mediator regulated by feeding

Fonseca, Fernando Rodrı́guez de; Navarro, Miguel; Gómez, R.; Escuredo, Leticia; Nava, Felice; Fu, Jin; Murillo-Rodrı́guez, Eric; Giuffrida, Andrea; LoVerme, Jesse; Gaetani, Silvana; Kathuria, S. P.; Gall, Christine M.; Piomelli, Daniele

doi:10.1038/35102582

Cited by 645 publications

(846 citation statements)

References 28 publications

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“…1J–K) (Video S1) and without, as described previously (Rodriguez de Fonseca et al. 2001; Proulx et al. 2005), inducing conditioned avoidance (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…2014), in ad libitum fed rats, the anorectic effect was almost exclusively due to a prolonged latency to eat (Rodriguez de Fonseca et al. 2001; Gaetani et al. 2003; Azari et al.…”

Section: Discussionmentioning

confidence: 99%

“…Rodriguez de Fonseca et al. (2001) argued for an involvement of sensory fibers of the abdominal vagus, but recent studies from our laboratory (Azari et al. 2014) challenge this concept.…”

Section: Introductionmentioning

confidence: 93%

“…2005; Rodriguez de Fonseca et al. 2001), but a high dose of IP OEA (20 mg/kg) was shown to impair locomotor activity in rats, a finding that was judged negligible in relation to the reduction in food intake (Rodriguez de Fonseca et al. 2001).…”

Section: Introductionmentioning

confidence: 99%

“…2001) and that vagal afferents are not necessary for the anorectic effect of OEA (Azari et al. 2014) indicated an alternative peripheral, vagus nerve‐independent, mechanism of action.…”

Section: Introductionmentioning

confidence: 99%

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Oleoylethanolamide-induced anorexia in rats is associated with locomotor impairment

et al. 2018

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The endogenous peroxisome proliferator‐activated receptor alpha (PPAR‐α) agonist Oleoylethanolamide (OEA) inhibits eating in rodents, mainly by delaying the onset of meals. The underlying mechanisms of OEA‐induced anorexia, however, remain unclear. Animals treated with high OEA doses were shown to display signs of discomfort and impaired locomotion. Therefore, we first examined whether the impaired locomotion may contribute to OEA's anorectic effect. Second, it is controversial whether abdominal vagal afferents are necessary for OEA's anorectic effect. Thus, we explored alternative peripheral neural pathways mediating IP OEA's anorectic effect by performing a celiac‐superior mesenteric ganglionectomy (CGX) or a subdiaphragmatic vagal deafferentation (SDA) alone or in combination. Exogenously administered OEA at a commonly used dose (10 mg/kg BW, IP) concurrently reduced food intake and compromised locomotor activity. Attempts to dissociate both phenomena using the dopamine D2/D3 receptor agonist Quinpirole (1 mg/kg BW, SC) failed because Quinpirole antagonized both, OEA‐induced locomotor impairment and delay in eating onset. CGX attenuated the prolongation of the latency to eat by IP OEA, but neither SDA nor CGX prevented IP OEA‐induced locomotor impairment. Our results indicate that IP OEA's anorectic effect may be secondary to impaired locomotion rather than due to physiological satiety. They further confirm that vagal afferents do not mediate exogenous OEA's anorectic effects, but suggest a role for spinal afferents in addition to an alternative, nonneuronal signaling route.

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“…1J–K) (Video S1) and without, as described previously (Rodriguez de Fonseca et al. 2001; Proulx et al. 2005), inducing conditioned avoidance (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…2014), in ad libitum fed rats, the anorectic effect was almost exclusively due to a prolonged latency to eat (Rodriguez de Fonseca et al. 2001; Gaetani et al. 2003; Azari et al.…”

Section: Discussionmentioning

confidence: 99%

“…Rodriguez de Fonseca et al. (2001) argued for an involvement of sensory fibers of the abdominal vagus, but recent studies from our laboratory (Azari et al. 2014) challenge this concept.…”

Section: Introductionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

“…2001) and that vagal afferents are not necessary for the anorectic effect of OEA (Azari et al. 2014) indicated an alternative peripheral, vagus nerve‐independent, mechanism of action.…”

Section: Introductionmentioning

confidence: 99%

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Oleoylethanolamide-induced anorexia in rats is associated with locomotor impairment

et al. 2018

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Oleoylethanolamide and Human Neural Responses to Food Stimuli in Obesity

et al. 2014

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IMPORTANCE Obesity has emerged as a leading health threat but its biological basis remains insufficiently known, hampering the search for novel treatments. Here, we study oleoylethanolamide, a naturally occurring lipid that has been clearly implicated in weight regulation in animals. However, its role for weight regulation and obesity in humans is still unclear.OBJECTIVE To investigate associations between plasma oleoylethanolamide levels and body mass index (BMI, calculated as weight in kilograms divided by height in meters squared) and functional magnetic resonance imaging response to food stimuli in obese patients and matched control participants. DESIGN, SETTING, AND PARTICIPANTSCase-control study of 21 obese patients and 24 matched control participants. Obesity was defined as having a BMI of at least 30. The mean age of participants was 40.8 years and BMIs ranged from 18.2 to 47.5. MAIN OUTCOMES AND MEASURESInteractions between plasma oleoylethanolamide levels and obesity on BMI and functional magnetic resonance imaging response to food stimuli.RESULTS Associations between oleoylethanolamide and BMI differed significantly depending on whether individuals were obese or not (P = .02). In obese individuals, oleoylethanolamide showed a trend toward a positive correlation with BMI (P = .06, ρ = 0.42), while this relationship was inverse for nonobese control participants (P = .07, ρ = −0.34). Similarly, we found significant interactions between oleoylethanolamide levels and obesity on food-related brain activation in cortical areas associated with reward processing and interoceptive signaling (P = .009). Specifically, nonobese individuals with higher oleoylethanolamide levels had higher insular brain activity (P < .001, ρ = 0.70); again, the relationship trended to be inverse for obese patients (P = .11, ρ = −0.36). These effects were not associated with plasma levels of leptin and anandamide, suggesting an independent role of oleoylethanolamide in hunger-associated interoceptive signaling. Analysis of food craving during the functional magnetic resonance imaging task suggested that the identified brain areas may be involved in suppressing food-liking reactions in nonobese individuals. CONCLUSIONS AND RELEVANCEThis study suggests that oleoylethanolamide-mediated signaling plays an important role for hedonic regulation of food craving and obesity in humans and thus may be a valuable target for developing novel antiobesity drugs.

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Anorexia

2004

Encyclopedic Dictionary of Genetics, Genomics and Proteomics

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An anorexic lipid mediator regulated by feeding

Cited by 645 publications

References 28 publications

Oleoylethanolamide-induced anorexia in rats is associated with locomotor impairment

Oleoylethanolamide-induced anorexia in rats is associated with locomotor impairment

Oleoylethanolamide and Human Neural Responses to Food Stimuli in Obesity

Anorexia

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