{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T19:20:24Z","timestamp":1787167224395,"version":"build-2736575974"},"reference-count":52,"publisher":"American Physiological Society","issue":"3","funder":[{"DOI":"10.13039\/501100010563","name":"Funds Baillet Latour","doi-asserted-by":"crossref","award":["Grant For Medical Research 2015"],"award-info":[{"award-number":["Grant For Medical Research 2015"]}],"id":[{"id":"10.13039\/501100010563","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100002661","name":"Fonds De La Recherche Scientifique - FNRS","doi-asserted-by":"publisher","award":["WELBIO-CR-2017C-02 and WELBIO-CR-2019C-02R"],"award-info":[{"award-number":["WELBIO-CR-2017C-02 and WELBIO-CR-2019C-02R"]}],"id":[{"id":"10.13039\/501100002661","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2020,9,1]]},"abstract":"<jats:p>\n                    Our objective was to explore the physiological role of the intestinal endocannabinoids in the regulation of appetite upon short-term exposure to high-fat-diet (HFD) and understand the mechanisms responsible for aberrant gut-brain signaling leading to hyperphagia in mice lacking Napepld in the intestinal epithelial cells (IECs). We generated a murine model harboring an inducible NAPE-PLD deletion in IECs ( Napepld\n                    <jats:sup>\u0394IEC<\/jats:sup>\n                    ). After an overnight fast, we exposed wild-type (WT) and Napepld\n                    <jats:sup>\u0394IEC<\/jats:sup>\n                    mice to different forms of lipid challenge (HFD or gavage), and we compared the modification occurring in the hypothalamus, in the vagus nerve, and at endocrine level 30 and 60 min after the stimulation. Napepld\n                    <jats:sup>\u0394IEC<\/jats:sup>\n                    mice displayed lower hypothalamic levels of N-oleoylethanolamine (OEA) in response to HFD. Lower mRNA expression of anorexigenic Pomc occurred in the hypothalamus of Napepld\n                    <jats:sup>\u0394IEC<\/jats:sup>\n                    mice after lipid challenge. This early hypothalamic alteration was not the consequence of impaired vagal signaling in Napepld\n                    <jats:sup>\u0394IEC<\/jats:sup>\n                    mice. Following lipid administration, WT and Napepld\n                    <jats:sup>\u0394IEC<\/jats:sup>\n                    mice had similar portal levels of glucagon-like peptide-1 (GLP-1) and similar rates of GLP-1 inactivation. Administration of exendin-4, a full agonist of GLP-1 receptor (GLP-1R), prevented the hyperphagia of Napepld\n                    <jats:sup>\u0394IEC<\/jats:sup>\n                    mice upon HFD. We conclude that in response to lipid, Napepld\n                    <jats:sup>\u0394IEC<\/jats:sup>\n                    mice displayed reduced OEA in brain and intestine, suggesting an impairment of the gut-brain axis in this model. We speculated that decreased levels of OEA likely contributes to reduce GLP-1R activation, explaining the observed hyperphagia in this model. Altogether, we elucidated novel physiological mechanisms regarding the gut-brain axis by which intestinal NAPE-PLD regulates appetite rapidly after lipid exposure.\n                  <\/jats:p>","DOI":"10.1152\/ajpendo.00146.2020","type":"journal-article","created":{"date-parts":[[2020,8,10]],"date-time":"2020-08-10T15:07:29Z","timestamp":1597072049000},"page":"E647-E657","source":"Crossref","is-referenced-by-count":20,"title":["Intestinal NAPE-PLD contributes to short-term regulation of food intake via gut-to-brain axis"],"prefix":"10.1152","volume":"319","author":[{"given":"Marialetizia","family":"Rastelli","sequence":"first","affiliation":[{"name":"Metabolism and Nutrition Research Group, Louvain Drug Research Institute, Walloon Excellence in Life sciences and BIOtechnology (WELBIO), UCLouvain, Universit\u00e9 catholique de Louvain, Bruxelles, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Van 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