{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T02:04:39Z","timestamp":1791252279476,"version":"4.1.0"},"reference-count":49,"publisher":"American Physiological Society","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2012,10,1]]},"abstract":"<jats:p>The antidiabetic intestinal L cell hormone glucagon-like peptide-1 (GLP-1) enhances glucose-dependent insulin secretion and inhibits gastric emptying. GLP-1 secretion is stimulated by luminal oleic acid (OA), which crosses the cell membrane by an unknown mechanism. We hypothesized that L cell fatty acid transport proteins (FATPs) are essential for OA-induced GLP-1 release. Therefore, the murine GLUTag L cell model was used for immunoblotting, [<jats:sup>3<\/jats:sup>H]OA uptake assay, and GLP-1 secretion assay as determined by radioimmunoassay following treatment with OA \u00b1 phloretin, sulfo- N-succinimidyl oleate, or siRNA against FATP4. FATP4<jats:sup>\u2212\/\u2212<\/jats:sup>and cluster-of-differentiation 36 (CD36)<jats:sup>\u2212\/\u2212<\/jats:sup>mice received intraileal OA, and plasma GLP-1 was measured by sandwich immunoassay. GLUTag cells were found to express CD36, FATP1, FATP3, and FATP4. The cells demonstrated specific<jats:sup>3<\/jats:sup>H[OA] uptake that was dose-dependently inhibited by 500 and 1,000 \u03bcM unlabeled OA ( P &lt; 0.001). Cell viability was not altered by treatment with OA. Phloretin and sulfo- N-succinimidyl oleate, inhibitors of protein-mediated transport and CD36, respectively, also decreased [<jats:sup>3<\/jats:sup>H]OA uptake, as did knockdown of FATP4 by siRNA transfection ( P &lt; 0.05\u20130.001). OA dose-dependently increased GLP-1 secretion at 500 and 1,000 \u03bcM ( P &lt; 0.001), whereas phloretin, sulfo- N-succinimidyl oleate, and FATP4 knockdown decreased this response ( P &lt; 0.05\u20130.01). FATP4<jats:sup>\u2212\/\u2212<\/jats:sup>mice displayed lower plasma GLP-1 at 60 min in response to intraileal OA ( P &lt; 0.05), whereas, unexpectedly, CD36<jats:sup>\u2212\/\u2212<\/jats:sup>mice displayed higher basal GLP-1 levels ( P &lt; 0.01) but a normal response to intraileal OA. Together, these findings demonstrate a key role for FATP4 in OA-induced GLP-1 secretion from the murine L cell in vitro and in vivo, whereas the precise role of CD36 remains unclear.<\/jats:p>","DOI":"10.1152\/ajpendo.00116.2012","type":"journal-article","created":{"date-parts":[[2012,8,8]],"date-time":"2012-08-08T05:46:49Z","timestamp":1344404809000},"page":"E899-E907","source":"Crossref","is-referenced-by-count":53,"title":["Role of fatty acid transport protein 4 in oleic acid-induced glucagon-like peptide-1 secretion from murine intestinal L cells"],"prefix":"10.1152","volume":"303","author":[{"given":"M. A.","family":"Poreba","sequence":"first","affiliation":[{"name":"Departments of Physiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. X.","family":"Dong","sequence":"additional","affiliation":[{"name":"Departments of Physiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. 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