ArticleThe Journal of biological chemistry2013
Phlorizin pretreatment reduces acute renal toxicity in a mouse model for diabetic nephropathy.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
- Myokine SIRPα exacerbates kidney disease in diabetes.JCI insight · 2026Article
- One year of hyperglycemia in the Ins2Akita mouse does not impart changes in retinal vascular patterning.PloS one · 2026Article
- Autophagy-lysosome flux failure in diabetic kidney disease: tubular vulnerability and cell-state remodeling.Frontiers in endocrinology · 2026Review
- Comparative study on muscle function in two different streptozotocin-induced diabetic models.Acta diabetologica · 2024Article
- Cocoa and Carob Supplementation, Alone or in Combination with Metformin, Protects against Hepatorenal Injury in Zucker Diabetic Fatty Rats.Nutrients · 2024Article
- Moderate beta-cell ablation triggers synergic compensatory mechanisms even in the absence of overt metabolic disruption.Communications biology · 2024Article
- Phlorizin, an Important Glucoside: Research Progress on Its Biological Activity and Mechanism.Molecules (Basel, Switzerland) · 2024Review
- Streptozotocin induces renal proximal tubular injury through p53 signaling activation.Scientific reports · 2023Article
- Transcription factor c-Maf deletion improves streptozotocin-induced diabetic nephropathy by directly regulating Sglt2 and Glut2.JCI insight · 2023Article
- A Review of Medicinal Plants with Renoprotective Activity in Diabetic Nephropathy Animal Models.Life (Basel, Switzerland) · 2023Review
- Treatment of tubular damage in high-fat-diet-fed obese mice using sodium-glucose co-transporter inhibitors.PloS one · 2023Article
- Dapagliflozin alleviates renal fibrosis in a mouse model of adenine-induced renal injury by inhibiting TGF-β1/MAPK mediated mitochondrial damage.Frontiers in pharmacology · 2023Article
- Dataset on biochemical markers and histological alterations in rat kidney intoxicated with cadmium chloride and treated with antioxidant.Data in brief · 2022Article
- Direct evidence of proximal tubular proliferation in early diabetic nephropathy.Scientific reports · 2022Article
- Serum Amyloid A3 Promoter-Driven Luciferase Activity Enables Visualization of Diabetic Kidney Disease.International journal of molecular sciences · 2022Article
- Streptozotocin-Induced Diabetes in a Mouse Model (BALB/c) Is Not an Effective Model for Research on Transplantation Procedures in the Treatment of Type 1 Diabetes.Biomedicines · 2021Article
- Angiotensin II up-regulates sodium-glucose co-transporter 2 expression and SGLT2 inhibitor attenuates Ang II-induced hypertensive renal injury in mice.Clinical science (London, England : 1979) · 2021Article
- Sodium-glucose co-transporter (SGLT) inhibitor restores lost axonal varicosities of the myenteric plexus in a mouse model of high-fat diet-induced obesity.Scientific reports · 2020Article
- The mechanisms of ameliorating effect of a green tea polyphenol on diabetic nephropathy based on diacylglycerol kinase α.Scientific reports · 2020Article
- Acute oral toxicity evaluation ofToxicology reports · 2019Article
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptozotocin (STZ) is widely used as diabetogenic agent in animal models for diabetic nephropathy (DN). However, it is also directly cytotoxic to kidneys, making it difficult to distinguish between DN-related and STZ-induced nephropathy. Therefore, an improved protocol to generate mice for DN studies, with a quick and robust achievement of the diabetic state, without direct kidney toxicity is required. To investigate the mechanism leading to STZ-induced nephropathy, kidney damage was induced with a high dose of STZ. This resulted in delayed gastric emptying, at least partially caused by impaired desacyl ghrelin clearance. STZ uptake in the kidneys is to a large extent mediated by the sodium/glucose cotransporters (Sglts) because the Sglt inhibitor phlorizin could reduce STZ uptake in the kidneys. Consequently, the direct toxic effects in the kidney and the gastric dilatation were resolved without interfering with the β-cell toxicity. Furthermore, pancreatic STZ uptake was increased, hereby decreasing the threshold for β-cell toxicity, allowing for single low non-nephrotoxic STZ doses (70 mg/kg). In conclusion, this study provides novel insights into the mechanism of STZ toxicity in kidneys and suggests a more efficient regime to induce DN with little or no toxic side effects.
Indexed as
Identifiers
What OpenQuestion holds
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.