{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T19:44:28Z","timestamp":1791315868216,"version":"4.3.1"},"reference-count":38,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2005,12,7]],"date-time":"2005-12-07T00:00:00Z","timestamp":1133913600000},"content-version":"vor","delay-in-days":6,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2005,12]]},"abstract":"<jats:p>\n                    The incretin hormone, glucagon\u2010like peptide\u20101 (GLP\u20101) is released from intestinal L\u2010cells following food ingestion. Its secretion is triggered by a range of nutrients, including fats, carbohydrates and proteins. We reported previously that Na\n                    <jats:sup>+<\/jats:sup>\n                    \u2010dependent glutamine uptake triggered electrical activity and GLP\u20101 release from the L\u2010cell model line GLUTag. However, whereas alanine also triggered membrane depolarization and GLP\u20101 secretion, the response was Na\n                    <jats:sup>+<\/jats:sup>\n                    independent. A range of alanine analogues, including\n                    <jats:sc>d<\/jats:sc>\n                    \u2010alanine, \u03b2\u2010alanine, glycine and\n                    <jats:sc>l<\/jats:sc>\n                    \u2010serine, but not\n                    <jats:sc>d<\/jats:sc>\n                    \u2010serine, triggered similar depolarizing currents and elevation of intracellular [Ca\n                    <jats:sup>2<\/jats:sup>\n                    <jats:sup>+<\/jats:sup>\n                    ], a sensitivity profile suggesting the involvement of glycine receptors. In support of this idea, glycine\u2010induced currents and GLP\u20101 release were blocked by strychnine, and currents showed a 58.5 mV shift in reversal potential per 10\u2010fold change in [Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    ], consistent with the activation of a Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    \u2010selective current. GABA, an agonist of related Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    channels, also triggered Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    currents and secretion, which were sensitive to picrotoxin. GABA\u2010triggered [Ca\n                    <jats:sup>2<\/jats:sup>\n                    <jats:sup>+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    increments were abolished by bicuculline and partially impaired by (1,2,5,6\u2010tetrahydropyridine\u20104\u2010yl)methylphosphinic acid (TPMPA), suggesting the involvement of both GABA\n                    <jats:sub>A<\/jats:sub>\n                    and GABA\n                    <jats:sub>C<\/jats:sub>\n                    receptors. Expression of GABA\n                    <jats:sub>A<\/jats:sub>\n                    , GABA\n                    <jats:sub>C<\/jats:sub>\n                    and glycine receptor subunits was confirmed by RT\u2010PCR. Glycine\u2010triggered GLP\u20101 secretion was impaired by bumetanide but not bendrofluazide, suggesting that a high intracellular [Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    ] maintained by Na\n                    <jats:sup>+<\/jats:sup>\n                    \u2013K\n                    <jats:sup>+<\/jats:sup>\n                    \u20132Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    cotransporters is necessary for the depolarizing response to glycine receptor ligands. Our results suggest that GABA and glycine stimulate electrical activity and GLP\u20101 release from GLUTag cells by ligand\u2010gated ion channel activation, a mechanism that might be important in responses to endogenous ligands from the enteric nervous system or dietary sources.\n                  <\/jats:p>","DOI":"10.1113\/jphysiol.2005.098962","type":"journal-article","created":{"date-parts":[[2005,10,13]],"date-time":"2005-10-13T20:14:15Z","timestamp":1129234455000},"page":"761-772","source":"Crossref","is-referenced-by-count":109,"title":["The neurotransmitters glycine and GABA stimulate glucagon\u2010like peptide\u20101 release from the GLUTag cell line"],"prefix":"10.1113","volume":"569","author":[{"given":"A.","family":"Gameiro","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"F.","family":"Reimann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. 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