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The roles of FFA2 and acetate have not been explored in ischemia\u2010reperfusion injury (IRI). We therefore examined the function of FFA2 and the therapeutic potential of acetate to reduce tissue injury in an acute model of intestinal IRI. The superior mesenteric artery of wild\u2010type (WT) and FFA2\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice was briefly occluded then reperfused following treatment with acetate or vehicle. The absence of FFA2 resulted in intestinal injury similar to that observed in WT mice, indicating a minimal causal role for FFA2 in this model. Acetate treatment to WT mice prior to ischemia profoundly protected the intestine from IRI\u2010induced damage. Amelioration of IRI was also observed, although to a lesser extent, when acetate was administered to FFA2\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice demonstrating that certain protective effects of acetate were FFA2\u2010independent. Remarkably, despite the lack of tissue damage following IRI, acetate\u2010treated mice had markedly increased neutrophil infiltration to the reperfused intestine which was dependent on FFA2. These studies reveal a minimal causal role for FFA2 in intestinal IRI but highlight the novel therapeutic potential for acetate in the amelioration of ischemia\u2010mediated tissue damage.\n                  <\/jats:p>","DOI":"10.1096\/fj.202000960r","type":"journal-article","created":{"date-parts":[[2020,7,29]],"date-time":"2020-07-29T14:14:30Z","timestamp":1596032070000},"page":"10418-10430","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Acetate protects against intestinal ischemia\u2010reperfusion injury independent of its cognate free fatty acid 2 receptor"],"prefix":"10.1096","volume":"34","author":[{"given":"Zoe V.","family":"Schofield","sequence":"first","affiliation":[{"name":"School of Biomedical Sciences The University of Queensland Brisbane QLD Australia"},{"name":"The Institute for Molecular Bioscience The University of Queensland Brisbane QLD Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mike C. 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