ArticleJournal of diabetes investigation2018
Ipragliflozin improves mitochondrial abnormalities in renal tubules induced by a high-fat diet.
Article in Journal of diabetes investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Effect of Insulin on Proximal Tubules Handling of Glucose: A Systematic Review.Journal of diabetes research · 2020Pooled it
- A metabolomics-based molecular pathway analysis of how the sodium-glucose co-transporter-2 inhibitor dapagliflozin may slow kidney function decline in patients with diabetes.Diabetes, obesity & metabolism · 2020 · on this mapTrial
- Insulin resistance and hyperinsulinaemia in kidney disease: mechanisms and metabolic effects.Nature reviews. Nephrology · 2026Review
- SGLT2 inhibitor dapagliflozin treats heart failure with preserved ejection fraction via the SIRT1/PGC-1α pathway.Acta biochimica et biophysica Sinica · 2026Article
- Canagliflozin Promotes Structural and Functional Changes in Proximal Tubular Cell Mitochondria of Hypertensive-Diabetic Mice.International journal of molecular sciences · 2025Article
- Chronic hyperglycemia and cardiovascular dysfunction: an in-depth exploration of metabolic and cellular pathways in type 2 diabetes mellitus.Cardiovascular diabetology. Endocrinology reports · 2025Review
- Dapagliflozin reduces proteinuria in IgA nephropathy patients receiving immunosuppressive therapy.Renal failure · 2025Article
- Cardiac Damage in Hypertension: From Molecular Mechanisms to Novel Therapeutic Approaches.International journal of molecular sciences · 2025Review
- The Role of Mitochondria in Diabetic Kidney Disease and Potential Therapeutic Targets.Kidney international reports · 2025Review
- Mitochondria and the Repurposing of Diabetes Drugs for Off-Label Health Benefits.International journal of molecular sciences · 2025Review
- SGLT2 inhibition and adipose tissue metabolism: current outlook and perspectives.Cardiovascular diabetology · 2024Review
- mTOR and SGLT-2 Inhibitors: Their Synergistic Effect on Age-Related Processes.International journal of molecular sciences · 2024Review
- Megalin Knockout Reduces SGLT2 Expression and Sensitizes to Western Diet-induced Kidney Injury.Function (Oxford, England) · 2024Article
- A Comprehensive Review of Emerging Therapies for Type 2 Diabetes and Their Cardiovascular Effects.Cureus · 2024Review
- New Molecules in Type 2 Diabetes: Advancements, Challenges and Future Directions.International journal of molecular sciences · 2024Review
- Association between different insulin resistance indices and all-cause mortality in patients with diabetic kidney disease: a prospective cohort study.Frontiers in endocrinology · 2024Article
- Insulin Resistance, Obesity, and Lipotoxicity.Advances in experimental medicine and biology · 2024Review
- Oxidative Stress Induced by Lipotoxicity and Renal Hypoxia in Diabetic Kidney Disease and Possible Therapeutic Interventions: Targeting the Lipid Metabolism and Hypoxia.Antioxidants (Basel, Switzerland) · 2023Review
- The potential mechanism of gut microbiota-microbial metabolites-mitochondrial axis in progression of diabetic kidney disease.Molecular medicine (Cambridge, Mass.) · 2023Review
- Mitochondrial Fission as a Therapeutic Target for Metabolic Diseases: Insights into Antioxidant Strategies.Antioxidants (Basel, Switzerland) · 2023Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
AIMS/
introductionComplete mechanisms of renoprotective effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors have not been elucidated yet. Mitochondrial biogenesis is regulated by membrane GTPases, such as optic atrophy factor 1 and mitofusion 2. Here, we investigated whether SGLT2 inhibition in mice fed with a high-fat diet (HFD) improved mitochondrial morphology and restored mitochondrial biogenesis-related molecules. MATERIALS AND
methodsMice were fed a control diet or HFD with or without ipragliflozin treatment. After 16 weeks, the kidneys were taken out and utilized for the analysis.
resultsHFD-fed mice treated with ipragliflozin showed increased caloric intake and ate more food than the control HFD-fed mice. Body and kidney weights, and blood glucose levels were not altered by ipragliflozin treatment in HFD-fed mice. Histological analysis showed that, compared with control mice, HFD-fed mice displayed tubular vacuolation, dilatation and epithelial cell detachment; ipragliflozin ameliorated these alterations. Furthermore, ultrastructural analysis showed that the tubule mitochondria of HFD-fed mice exhibited significant damage. Again, ipragliflozin reversed the damage to a normal state, and restored optic atrophy factor 1 and mitofusion 2 levels in HFD-fed mice. Increased urine 8-hydroxydeoxyguanosine levels in HFD-fed mice were suppressed by ipragliflozin as well. In vitro experiments using HK-2 cells revealed that either high glucose or high palmitate suppressed optic atrophy factor 1 and mitofusion 2 levels. Suppression of SGLT2 by a specific small interfering ribonucleic acid or ipragliflozin restored these GTPase levels to their normal values.
conclusionsSGLT2 inhibition might act directly on tubular cells and protect kidney tubular cells from mitochondrial damage by metabolic insults regardless of blood glucose levels or improvement in bodyweight reduction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.