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    Oleoyl-lysophosphatidylinositol enhances glucagon-like peptide-1 secretion from enteroendocrine L-cells through GPR119.

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    Authors
    Arifin, S.
    Paternoster, Silvano
    Carlessi, Rodrigo
    Casari, Ilaria
    Ekberg, J.
    Maffucci, T.
    Newsholme, Philip
    Rosenkilde, M.
    Falasca, Marco
    Date
    2018
    Type
    Journal Article
    
    Metadata
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    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.
    Source Title
    Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
    DOI
    10.1016/j.bbalip.2018.06.007
    ISSN
    0006-3002
    School
    School of Pharmacy and Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/68737
    Collection
    • Curtin Research Publications
    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.

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