title: Feeding-induced oleoylethanolamide mobilization is disrupted in the gut of diet-induced obese rodents.
abstract: The gastrointestinal tract plays a critical role in the regulation of energy homeostasis by initiating neural and hormonal responses to the ingestion of nutrients. In addition to peptide hormones, such as cholecystokinin (CKK) and peptide YY (PYY), the lipid-derived mediator oleoylethanolamide (OEA) has been implicated in the control of satiety. Previous studies in humans and rodent models have shown that obesity is associated with changes in CCK, PYY and other gut-derived peptide hormones, which may contribute to decreased satiety and increased energy intake. In the present study, we show that small-intestinal OEA production is disrupted in the gut of diet-induced obese (DIO) rats and mice. In lean rodents, feeding or duodenal infusion of Intralipid® or pure oleic acid stimulates jejunal OEA mobilization. This response is strikingly absent in DIO rats and mice. Confirming previous reports, we found that feeding rats or mice a high-fat diet for 7 days is sufficient to suppress jejunal OEA mobilization. Surprisingly, a similar effect is elicited by feeding rats and mice a high-sucrose low-fat diet for 7 days. Collectively, our findings suggest that high fat-induced obesity is accompanied by alterations in the post-digestive machinery responsible for OEA biosynthesis, which may contribute to reduced satiety and hyperphagia.
authors.affiliation: Department of Anatomy and Neurobiology, University of California, Irvine, CA, USA.
authors.forename: Miki
authors.initials: M
authors.lastname: Igarashi
authors.affiliation: Department of Anatomy and Neurobiology, University of California, Irvine, CA, USA.
authors.forename: Nicholas V
authors.initials: NV
authors.lastname: DiPatrizio
authors.affiliation: Department of Anatomy and Neurobiology, University of California, Irvine, CA, USA.
authors.forename: Vidya
authors.initials: V
authors.lastname: Narayanaswami
authors.affiliation: Department of Anatomy and Neurobiology, University of California, Irvine, CA, USA; Drug Discovery and Development, Istituto Italiano di Tecnologia, Genova, Italy. Electronic address: piomelli@uci.edu.
authors.forename: Daniele
authors.initials: D
authors.lastname: Piomelli
mesh_terms: D000818:Animals; D001692:Biological Transport; D059305:Diet, High-Fat / Q000009:adverse effects*; D004040:Dietary Carbohydrates / Q000009:adverse effects; D004041:Dietary Fats / Q000008:administration & dosage; D004386:Duodenum / Q000378:metabolism* / Q000503:physiopathology; D004435:Eating; D063388:Endocannabinoids / Q000378:metabolism*; D006963:Hyperphagia / Q000378:metabolism / Q000473:pathology; D007583:Jejunum / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D009829:Oleic Acids / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012527:Satiation; D013395:Sucrose / Q000008:administration & dosage
chemical_list: D004040:Dietary Carbohydrates; D004041:Dietary Fats; D063388:Endocannabinoids; D009829:Oleic Acids; C488250:oleoylethanolamide; D013395:Sucrose
keywords: Diet-induced obesity; Dietary fat; Linoleoylethanolamide; Oleoylethanolamide; Satiety