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GPCRs are involved in regulating glucose\u2010stimulated insulin secretion (GSIS). Previous studies have suggested that PLC\u2010\u03b2s might play an important role in pancreatic \u03b2 cells. However, because of a lack of the specific inhibitors of PLC\u2010\u03b2 isozymes and appropriate genetic models, the\n                    <jats:italic>in vivo<\/jats:italic>\n                    function of specific PLC\u2010\u03b2 isozymes in pancreatic \u03b2 cells and their physiologic relevance in the regulation of insulin secretion have not been studied so far. The present study showed that PLC\u2010\u03b21 was crucial for \u03b2\u2010cell function by generation of each PLC\u2010\u03b2 conditional knockout mouse. Mice lacking PLC\u2010\u03b21 in \u03b2 cells exhibited a marked defect in GSIS, leading to glucose intolerance. In\n                    <jats:italic>ex vivo<\/jats:italic>\n                    studies, the secreted insulin level and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    response in\n                    <jats:italic>\n                      Plcb1\n                      <jats:sup>f\/f<\/jats:sup>\n                      ;\n                    <\/jats:italic>\n                    pancreas\/duodenum homeobox protein 1 (\n                    <jats:italic>Pdx1<\/jats:italic>\n                    )\u2010Cre recombinase\u2010estrogen receptor T2 (\n                    <jats:italic>CreERt2<\/jats:italic>\n                    ) islets was lower than those in the\n                    <jats:italic>\n                      Plcb1\n                      <jats:sup>f\/f<\/jats:sup>\n                    <\/jats:italic>\n                    islets under the high\u2010glucose condition. PLC\u2010\u03b21 led to potentiate insulin secretion\n                    <jats:italic>via<\/jats:italic>\n                    stimulation of particular G\n                    <jats:sub>q<\/jats:sub>\n                    \u2010protein\u2013coupled receptors.\n                    <jats:italic>\n                      Plcb1\n                      <jats:sup>f\/f<\/jats:sup>\n                      ; Pdx1\u2010CreERt2\n                    <\/jats:italic>\n                    mice fed a high\u2010fat diet developed more severe glucose intolerance because of a defect in insulin secretion. The present study identified PLC\u2010\u03b21 as an important molecule that regulates \u03b2 cell insulin secretion and can be considered a candidate for therapeutic intervention in diabetes mellitus.\u2014Hwang, H.\u2010J., Yang, Y. R., Kim, H. Y., Choi, Y., Park, K.\u2010S., Lee, H., Ma, J. S., Yamamoto, M., Kim, J., Chae, Y. C., Choi, J. H., Coceo, L., Berggren, P.\u2010O., Jang, H.\u2010J., Suh, P.\u2010G. Phospholipase C\u03b21 potentiates glucose\u2010stimulated insulin secretion. FASEB J. 33, 10668\u201310679 (2019).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201802732rr","type":"journal-article","created":{"date-parts":[[2019,7,3]],"date-time":"2019-07-03T14:10:00Z","timestamp":1562163000000},"page":"10668-10679","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Phospholipase C\u2010\u03b21 potentiates glucose\u2010stimulated insulin secretion"],"prefix":"10.1096","volume":"33","author":[{"given":"Hyeon-Jeong","family":"Hwang","sequence":"first","affiliation":[{"name":"School of Life Sciences Ulsan National Institute of Science and Technology Ulsan South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yong Ryoul","family":"Yang","sequence":"additional","affiliation":[{"name":"Aging Research Center Korea 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