ArticleDiabetes2014
Podocyte-specific GLUT4-deficient mice have fewer and larger podocytes and are protected from diabetic nephropathy.
Article in Diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 58 citations in OpenAlex.
- AMPK is dispensable for physiological podocyte and glomerular functions but prevents glomerular fibrosis in experimental diabetes.Cell death discovery · 2026Article
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- A static glucose-stimulated insulin secretion (sGSIS) assay that is significantly predictive of time to diabetes reversal in the human islet bioassay.BMJ open diabetes research & care · 2024Article
- Single-Cell Transcriptional Landscape Reveals the Regulatory Network and Its Heterogeneity of Renal Mitochondrial Damages in Diabetic Kidney Disease.International journal of molecular sciences · 2023Article
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- The role of protein tyrosine phosphatase 1B (PTP1B) in the pathogenesis of type 2 diabetes mellitus and its complications.Journal of physiology and biochemistry · 2022Review
- Podocyte Bioenergetics in the Development of Diabetic Nephropathy: The Role of Mitochondria.Endocrinology · 2022Review
- Mitochondria in Diabetic Kidney Disease.Cells · 2021Review
- GPR43 deficiency protects against podocyte insulin resistance in diabetic nephropathy through the restoration of AMPKα activity.Theranostics · 2021Article
- Baicalin reversal of DNA hypermethylation-associated Klotho suppression ameliorates renal injury in type 1 diabetic mouse model.Cell cycle (Georgetown, Tex.) · 2020Article
- Critical Role for AMPK in Metabolic Disease-Induced Chronic Kidney Disease.International journal of molecular sciences · 2020Review
- SGLT2 Inhibitor Empagliflozin and DPP4 Inhibitor Linagliptin Reactivate Glomerular Autophagy inInternational journal of molecular sciences · 2020Article
- Podocyte Lysosome Dysfunction in Chronic Glomerular Diseases.International journal of molecular sciences · 2020Review
- Yu Nu Compound Regulates Autophagy and Apoptosis Through mTOR in vivo and vitro.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- Lipid mediators of insulin signaling in diabetic kidney disease.American journal of physiology. Renal physiology · 2019Review
- The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes.Kidney international · 2019Article
- SMPDL3b modulates insulin receptor signaling in diabetic kidney disease.Nature communications · 2019Article
- Ion channels and transporters in diabetic kidney disease.Current topics in membranes · 2019Review
- The SLC transporter in nutrient and metabolic sensing, regulation, and drug development.Journal of molecular cell biology · 2019Article
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Authors and funding
21 authors at 5 institutions in 2 countries.
Funding
Abstract
Podocytes are a major component of the glomerular filtration barrier, and their ability to sense insulin is essential to prevent proteinuria. Here we identify the insulin downstream effector GLUT4 as a key modulator of podocyte function in diabetic nephropathy (DN). Mice with a podocyte-specific deletion of GLUT4 (G4 KO) did not develop albuminuria despite having larger and fewer podocytes than wild-type (WT) mice. Glomeruli from G4 KO mice were protected from diabetes-induced hypertrophy, mesangial expansion, and albuminuria and failed to activate the mammalian target of rapamycin (mTOR) pathway. In order to investigate whether the protection observed in G4 KO mice was due to the failure to activate mTOR, we used three independent in vivo experiments. G4 KO mice did not develop lipopolysaccharide-induced albuminuria, which requires mTOR activation. On the contrary, G4 KO mice as well as WT mice treated with the mTOR inhibitor rapamycin developed worse adriamycin-induced nephropathy than WT mice, consistent with the fact that adriamycin toxicity is augmented by mTOR inhibition. In summary, GLUT4 deficiency in podocytes affects podocyte nutrient sensing, results in fewer and larger cells, and protects mice from the development of DN. This is the first evidence that podocyte hypertrophy concomitant with podocytopenia may be associated with protection from proteinuria.
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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 Socratic graph.