ArticleClinical and experimental nephrology2023
Canagliflozin protects the cardiovascular system through effects on the gut environment in non-diabetic nephrectomized rats.
Article in Clinical and experimental nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Canagliflozin attenuates Parkinson's disease and is associated with modulation of gut-inflammasome-brain axis in rats.Inflammopharmacology · 2026Article
- Pharmacomicrobiomics in metabolic syndrome and type 2 diabetes: the microbiome-drug-host triad.Frontiers in pharmacology · 2026Review
- A guide to uraemic toxicity.Nature reviews. Nephrology · 2026Review
- Gut microbiota's role in heart failure.Heart failure reviews · 2025Review
- Targeting Neurodegeneration with SGLT2is: From Molecular Mechanisms to Clinical Implications.Molecular neurobiology · 2025Review
- Article
- Kidney-Gut Axis in Chronic Kidney Disease: Therapeutic Perspectives from Microbiota Modulation and Nutrition.Nutrients · 2025Review
- The impact of sodium-glucose cotransporter inhibitors on gut microbiota: a scoping review.Journal of diabetes and metabolic disorders · 2024Article
- Antibacterial Activity and Mechanism of Canagliflozin against Methicillin-ResistantMolecules (Basel, Switzerland) · 2023Article
- Gut microbiota interactions with anti-diabetic medications and pathogenesis of type 2 diabetes mellitus.World journal of methodology · 2022Review
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
backgroundThe gut produces toxins that contribute to the cardiovascular complications of chronic kidney disease. Canagliflozin, a sodium glucose cotransporter (SGLT) 2 inhibitor that is used as an anti-diabetic drug, has a weak inhibitory effect against SGLT1 and may affect the gut glucose concentration and environment.
methodsHere, we determined the effect of canagliflozin on the gut microbiota and the serum gut-derived uremic toxin concentrations in 5/6th nephrectomized (Nx) rats.
resultsCanagliflozin increased the colonic glucose concentration and restored the number of Lactobacillus bacteria, which was low in Nx rats. In addition, the expression of tight junction proteins in the ascending colon was low in Nx rats, and this was partially restored by canagliflozin. Furthermore, the serum concentrations of gut-derived uremic toxins were significantly increased by Nx and reduced by canagliflozin. Finally, the wall of the thoracic aorta was thicker and there was more cardiac interstitial fibrosis in Nx rats, and these defects were ameliorated by canagliflozin.
conclusionsThe increases in colonic glucose concentration, Lactobacillus numbers and tight junction protein expression, and the decreases in serum uremic toxin concentrations and cardiac interstitial fibrosis may have been caused by the inhibition of SGLT1 by canagliflozin because similar effects were not identified in tofogliflozin-treated rats.
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