| First Author | Caillon A | Year | 2018 |
| Journal | Metabolism | Volume | 87 |
| Pages | 13-17 | PubMed ID | 29936173 |
| Mgi Jnum | J:321704 | Mgi Id | MGI:6884298 |
| Doi | 10.1016/j.metabol.2018.06.005 | Citation | Caillon A, et al. (2018) The OEA effect on food intake is independent from the presence of PPARalpha in the intestine and the nodose ganglion, while the impact of OEA on energy expenditure requires the presence of PPARalpha in mice. Metabolism 87:13-17 |
| abstractText | BACKGROUND: Oleoylethanolamide (OEA) is an endocannabinoid that controls food intake, energy expenditure and locomotor activity. Its anorexigenic effect appears to be mediated by PPARalpha, but the tissue where the presence of this receptor is required for OEA to inhibit feeding is unknown as yet. Previous studies point to a possible role of proximal enterocytes and neurons of the nodose ganglion. MATERIALS AND METHODS: Acute intraperitoneal OEA effects on food intake, energy expenditure, respiratory exchange ratio (RER) and locomotor activity were studied in control mice (PPARalpha-loxP) and intestinal (Villin-Cre;PPARalpha-loxP) or nodose ganglion (Phox2B-Cre;PPARalpha-loxP) specific PPARalpha knockout mice placed in calorimetric cages. RESULTS: OEA administration to both intestinal and nodose ganglion PPARalpha knockout mice decreased food intake, RER (leading to increased lipid oxidation) and locomotor activity as in control mice. However, while OEA injection acutely decreased energy expenditure in controls, this effect was not observed in mice devoid of PPARalpha in the intestine. CONCLUSION: These results indicate that the OEA effect on food intake is independent from the presence of PPARalpha in the intestine and the nodose ganglion, while the impact of OEA on energy expenditure requires the presence of PPARalpha in the intestine. |
