ArticleJournal of veterinary internal medicine2026
Effect of canagliflozin treatment on β-cell responsiveness in insulin-dysregulated horses: a 4-week, multi-arm, double-blind, randomized clinical trial.
Article in Journal of veterinary internal medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
7 authors.
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Abstract
backgroundThe sodium-glucose co-transporter 2 (SGLT2) inhibitor canagliflozin (CAN) decreases hyperinsulinemia in insulin-dysregulated (ID) horses, but its effects on pancreatic β-cell responsiveness to glucose are unknown. HYPOTHESIS/
objectivesCompare the effects of 2 CAN dosages (0.6 and 1.2 mg/kg) with placebo (PBO) on β-cell responsiveness to IV glucose in ID horses using a graded glucose infusion (GGI) test. ANIMALS: Forty-two privately-owned ID horses.
methodsRandomized, multicenter, double-blind, parallel-group, multi-arm, PBO-controlled study. Horses underwent GGI testing before and after 4 weeks of treatment with PO CAN (0.6 or 1.2 mg/kg) or PBO. Indices of β-cell responsiveness included the slope of insulin vs glucose relationship (ΔI vs ΔG) and the ratio of the incremental areas under the curve for insulin and glucose (iAUCINS/iAUCGLU).
resultsLeast squares (LS) means ± SEM ΔI vs ΔG values were lower with CAN (0.6 and 1.2 mg/kg) than with PBO (P ≤ .001; 22.0 ± 3.5 and 21.1 ± 3.2 mIU/mmol vs 38.4 ± 3.3 mIU/mmol) with no difference between CAN dosages (P = .96). Geometric LS mean (95% CI) iAUCINS/iAUCGLU values were lower with CAN (0.6 and 1.2 mg/kg) compared with PBO (P ≤ .001; 19.3 [16.5-22.5] and 16.4 [13.9-19.3] mIU/mmol vs 33.1 [28.4-38.7] mIU/mmol). CONCLUSIONS AND CLINICAL IMPORTANCE: Canagliflozin decreased β-cell responsiveness to IV glucose in ID horses, representing a key mechanism underlying the hyperinsulinemia-decreasing effect of SGLT2 treatment in horses.
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