ArticleAmerican journal of physiology. Renal physiology2013
Knockout of Na-glucose transporter SGLT2 attenuates hyperglycemia and glomerular hyperfiltration but not kidney growth or injury in diabetes mellitus.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers, 3 of them syntheses that pooled it.
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Who cites it
199 citing papers in PubMed, 3 syntheses or guidelines pooled it, 366 citations in OpenAlex.
- Acute kidney injury events in patients with diabetes using sodium glucose transporter 2 inhibitors: a meta-analysis of cohort studies.Acta diabetologica · 2024Pooled it
- Effect of Insulin on Proximal Tubules Handling of Glucose: A Systematic Review.Journal of diabetes research · 2020Pooled it
- Effect of SGLT2 inhibitor on renal function in patients with type 2 diabetes mellitus: a systematic review and meta-analysis of randomized controlled trials.International urology and nephrology · 2019Pooled it
- Renal effects of a sodium-glucose cotransporter 2 inhibitor, tofogliflozin, in relation to sodium intake and glycaemic status.Diabetes, obesity & metabolism · 2019Trial
- Metabolic response to sodium-glucose cotransporter 2 inhibition in type 2 diabetic patients.The Journal of clinical investigation · 2014 · on this mapTrial
- Proteomics analysis of empagliflozin in patients without diabetes or overt heart failure from empagliflozin and cardiac remodeling in people without diabetes CardioLink-7 randomized clinical trial.Cardiovascular endocrinology & metabolism · 2026Article
- The SGLT2i "canagliflozin" and the DPP-4i "sitagliptin" mitigate hypertensive nephropathy in adult male rats by modulating the Ang II/RAGE/Nox4/NLRP3 cascade.Frontiers in physiology · 2026Article
- Canagliflozin Promotes Structural and Functional Changes in Proximal Tubular Cell Mitochondria of Hypertensive-Diabetic Mice.International journal of molecular sciences · 2025Article
- Sodium-Glucose Cotransporter-2 Inhibitors in Diabetes and Beyond: Mechanisms, Pleiotropic Benefits, and Clinical Use-Reviewing Protective Effects Exceeding Glycemic Control.Molecules (Basel, Switzerland) · 2025Review
- From Current Therapeutics to Multitarget Ligands: A Review of Diabetes Pharmacological Treatments.Pharmaceutics · 2025Review
- Induction of proximal tubular proliferation and lengthening in response to sodium glucose linked cotransporter-2 inhibition in experimental rats.Journal of diabetes investigation · 2025Article
- ASK1 limits kidney glucose reabsorption, growth, and mid-late proximal tubule KIM-1 induction when diabetes and Western diet are combined with SGLT2 inhibition.American journal of physiology. Renal physiology · 2025Article
- Effects of sotagliflozin on kidney and cardiac outcome in a hypertensive model of subtotal nephrectomy in male mice.Physiological reports · 2025Article
- Analysing the influence of dapagliflozin on urinary tract infection vulnerability and kidney injury in mice infected with uropathogenic Escherichia coli.Diabetes, obesity & metabolism · 2025Article
- Placenta-derived mesenchymal stem cells protect against diabetic kidney disease by upregulating autophagy-mediated SIRT1/FOXO1 pathway.Renal failure · 2024Article
- State-of-the-Art-Review: Mechanisms of Action of SGLT2 Inhibitors and Clinical Implications.American journal of hypertension · 2024Review
- Elevated urinary albumin predicts increased time in range after initiation of SGLT2 inhibitors in individuals with type 1 diabetes on sensor-augmented pump therapy.Diabetology international · 2024Article
- Modern Challenges in Type 2 Diabetes: Balancing New Medications with Multifactorial Care.Biomedicines · 2024Review
- Inhibition of STIM1 alleviates high glucose-induced proliferation and fibrosis by inducing autophagy in mesangial cells.Molecular and cellular biochemistry · 2024Article
- Transporter Proteins as Therapeutic Drug Targets-With a Focus on SGLT2 Inhibitors.International journal of molecular sciences · 2024Review
139 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
The Na-glucose cotransporter SGLT2 mediates high-capacity glucose uptake in the early proximal tubule and SGLT2 inhibitors are developed as new antidiabetic drugs. We used gene-targeted Sglt2 knockout (Sglt2(-/-)) mice to elucidate the contribution of SGLT2 to blood glucose control, glomerular hyperfiltration, kidney growth, and markers of renal growth and injury at 5 wk and 4.5 mo after induction of low-dose streptozotocin (STZ) diabetes. The absence of SGLT2 did not affect renal mRNA expression of glucose transporters SGLT1, NaGLT1, GLUT1, or GLUT2 in response to STZ. Application of STZ increased blood glucose levels to a lesser extent in Sglt2(-/-) vs. wild-type (WT) mice (∼300 vs. 470 mg/dl) but increased glucosuria and food and fluid intake to similar levels in both genotypes. Lack of SGLT2 prevented STZ-induced glomerular hyperfiltration but not the increase in kidney weight. Knockout of SGLT2 attenuated the STZ-induced renal accumulation of p62/sequestosome, an indicator of impaired autophagy, but did not attenuate the rise in renal expression of markers of kidney growth (p27 and proliferating cell nuclear antigen), oxidative stress (NADPH oxidases 2 and 4 and heme oxygenase-1), inflammation (interleukin-6 and monocyte chemoattractant protein-1), fibrosis (fibronectin and Sirius red-sensitive tubulointerstitial collagen accumulation), or injury (renal/urinary neutrophil gelatinase-associated lipocalin). SGLT2 deficiency did not induce ascending urinary tract infection in nondiabetic or diabetic mice. The results indicate that SGLT2 is a determinant of hyperglycemia and glomerular hyperfiltration in STZ-induced diabetes mellitus but is not critical for the induction of renal growth and markers of renal injury, inflammation, and fibrosis.
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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.