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. 2023 Dec 28;149(11):860–884. doi: 10.1161/CIRCULATIONAHA.123.065517

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© 2023 The Authors.

Circulation is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 3. — Untargeted metabolome analysis reveals SGLT2i-induced alterations in amino acid and organic anion metabolism. A, Overview of untargeted metabolomics results in wild-type (WT) and diabetic Akita mice. Significant metabolites from >30 000 quantified features with breakdown of altered metabolites by organ and genotype. B, The metabolite pool is sensitive to changes in production as well as kidney secretion and reabsorption. C, Illustration of interorgan communication by linking solute carrier group (SLCs) downregulated in the kidney to enhanced urinary metabolites and depleted metabolites in other organs. D, SGLT2 (sodium-glucose cotransporter 2)–dependent changes in plasma:urine ratios indicate increased urinary excretion of glucose and glucose metabolites, and less secretion of substrates of the kidney organic anion transporters (see text for details). Urine metabolites were normalized to creatinine. E, Immunoblot analysis of OAT1 (organic anion transporter 1) in SGLT2i-treated WT mice shows reduction of OAT1 (Slc22a6; normalized to b-actin; 2-sided t test), consistent with proteomics results. F, Targeted analysis of microbiota-derived organic anions (uremic toxins) in the plasma of WT and diabetic Akita mice. RBC indicates red blood cell.