Oleoyl-lysophosphatidylinositol enhances glucagon-like peptide-1 secretion from enteroendocrine L-cells through GPR119.
dc.contributor.author | Arifin, S. | |
dc.contributor.author | Paternoster, Silvano | |
dc.contributor.author | Carlessi, Rodrigo | |
dc.contributor.author | Casari, Ilaria | |
dc.contributor.author | Ekberg, J. | |
dc.contributor.author | Maffucci, T. | |
dc.contributor.author | Newsholme, Philip | |
dc.contributor.author | Rosenkilde, M. | |
dc.contributor.author | Falasca, Marco | |
dc.date.accessioned | 2018-06-29T12:27:00Z | |
dc.date.available | 2018-06-29T12:27:00Z | |
dc.date.created | 2018-06-29T12:09:04Z | |
dc.date.issued | 2018 | |
dc.identifier.citation | Arifin, S. and Paternoster, S. and Carlessi, R. and Casari, I. and Ekberg, J. and Maffucci, T. and Newsholme, P. et al. 2018. Oleoyl-lysophosphatidylinositol enhances glucagon-like peptide-1 secretion from enteroendocrine L-cells through GPR119. Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids. 1863 (9): pp. 1132-1141. | |
dc.identifier.uri | http://hdl.handle.net/20.500.11937/68737 | |
dc.identifier.doi | 10.1016/j.bbalip.2018.06.007 | |
dc.description.abstract |
The gastrointestinal tract is increasingly viewed as critical in controlling glucose metabolism, because of its role in secreting multiple glucoregulatory hormones, such as glucagon like peptide-1 (GLP-1). Here we investigate the molecular pathways behind the GLP-1- and insulin-secreting capabilities of a novel GPR119 agonist, Oleoyl-lysophosphatidylinositol (Oleoyl-LPI). Oleoyl-LPI is the only LPI species able to potently stimulate the release of GLP-1 in vitro, from murine and human L-cells, and ex-vivo from murine colonic primary cell preparations. Here we show that Oleoyl-LPI mediates GLP-1 secretion through GPR119 as this activity is ablated in cells lacking GPR119 and in colonic primary cell preparation from GPR119-/- mice. Similarly, Oleoyl-LPI-mediated insulin secretion is impaired in islets isolated from GPR119-/- mice. On the other hand, GLP-1 secretion is not impaired in cells lacking GPR55 in vitro or in colonic primary cell preparation from GPR55-/- mice. We therefore conclude that GPR119 is the Oleoyl-LPI receptor, upstream of ERK1/2 and cAMP/PKA/CREB pathways, where primarily ERK1/2 is required for GLP-1 secretion, while CREB activation appears dispensable. | |
dc.title | Oleoyl-lysophosphatidylinositol enhances glucagon-like peptide-1 secretion from enteroendocrine L-cells through GPR119. | |
dc.type | Journal Article | |
dcterms.source.issn | 0006-3002 | |
dcterms.source.title | Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids | |
curtin.department | School of Pharmacy and Biomedical Sciences | |
curtin.accessStatus | Fulltext not available |
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