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However, the underlying mechanism remains unclear. In this study, we aimed to use multiomics to identify the mediators involved in \u03b2-cell regeneration induced by dapagliflozin. We showed that dapagliflozin lowered blood glucose level, upregulated plasma insulin level, and increased islet area in db\/db mice. Dapagliflozin reshaped gut microbiota and modulated microbiotic and plasmatic metabolites related to tryptophan metabolism, especially l-tryptophan, in the diabetic mice. Notably, l-tryptophan upregulated the mRNA level of glucagon-like peptide 1 (GLP-1) production\u2013related gene (Gcg and Pcsk1) expression and promoted GLP-1 secretion in cultured mouse intestinal L cells, and it increased the supernatant insulin level in primary human islets, which was eliminated by GPR142 antagonist. Transplant of fecal microbiota from dapagliflozin-treated mice, supplementation of l-tryptophan, or treatment with dapagliflozin upregulated l-tryptophan, GLP-1, and insulin or C-peptide levels and promoted \u03b2-cell regeneration in db\/db mice. Addition of exendin 9-39, a GLP-1 receptor (GLP-1R) antagonist, or pancreatic Glp1r knockout diminished these beneficial effects. In summary, treatment with dapagliflozin in type 2 diabetic mice promotes \u03b2-cell regeneration by upregulating GLP-1 production, which is mediated via gut microbiota and tryptophan metabolism.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Article Highlights<\/jats:title>\n                  <\/jats:sec>","DOI":"10.2337\/db23-0553","type":"journal-article","created":{"date-parts":[[2024,3,12]],"date-time":"2024-03-12T14:49:58Z","timestamp":1710254998000},"page":"926-940","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":43,"title":["Gut Microbiota\u2212Tryptophan Metabolism\u2212GLP-1 Axis Participates in \u03b2-Cell Regeneration Induced by Dapagliflozin"],"prefix":"10.2337","volume":"73","author":[{"given":"Yafei","family":"Jiang","sequence":"first","affiliation":[{"name":"1Department of Endocrinology and Metabolism, State Key Laboratory of Female Fertility 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