ArticleAmerican journal of physiology. Renal physiology2010
Transgenic overexpression of GLUT1 in mouse glomeruli produces renal disease resembling diabetic glomerulosclerosis.
Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.
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Who cites it
21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.
- The contribution of genetic variants of SLC2A1 gene in T2DM and T2DM-nephropathy: association study and meta-analysis.Renal failure · 2018Pooled it
- Relationship between five GLUT1 gene single nucleotide polymorphisms and diabetic nephropathy: a systematic review and meta-analysis.Molecular biology reports · 2012Pooled it
- Persimmon carotenoid extract rich in β-cryptoxanthin improves glucose homeostasis and reduces liver damage in high-fat-diet-induced type 2 diabetic and metabolic dysfunction-associated steatotic liver disease mice.Journal of the science of food and agriculture · 2026Article
- Kidney Gastrin/CCKBR Attenuates Type 2 Diabetes Mellitus by Inhibiting SGLT2-Mediated Glucose Reabsorption through Erk/NF-κB Signaling Pathway.Diabetes & metabolism journal · 2025Article
- Single-cell transcriptomics reveals a mechanosensitive injury signaling pathway in early diabetic nephropathy.Genome medicine · 2023Article
- Molecular mechanisms underlying the role of hypoxia-inducible factor-1 α in metabolic reprogramming in renal fibrosis.Frontiers in endocrinology · 2022Review
- Revisiting Experimental Models of Diabetic Nephropathy.International journal of molecular sciences · 2020Review
- Angiopoietin-1 Promotes the Integrity of Neovascularization in the Subcutaneous Matrigel of Type 1 Diabetic Rats.BioMed research international · 2019Article
- Ion channels and transporters in diabetic kidney disease.Current topics in membranes · 2019Review
- Article
- FXR/TGR5 Dual Agonist Prevents Progression of Nephropathy in Diabetes and Obesity.Journal of the American Society of Nephrology : JASN · 2018Article
- Glucose Transporters in Diabetic Kidney Disease-Friends or Foes?Frontiers in endocrinology · 2018Review
- HIF-1 Mediates Renal Fibrosis in OVE26 Type 1 Diabetic Mice.Diabetes · 2016Article
- Kidney glycosphingolipids are elevated early in diabetic nephropathy and mediate hypertrophy of mesangial cells.American journal of physiology. Renal physiology · 2015Article
- Insulin signaling: implications for podocyte biology in diabetic kidney disease.Current opinion in nephrology and hypertension · 2015Article
- Podocytes, signaling pathways, and vascular factors in diabetic kidney disease.Advances in chronic kidney disease · 2014Review
- Podocyte-specific GLUT4-deficient mice have fewer and larger podocytes and are protected from diabetic nephropathy.Diabetes · 2014Article
- Associations between structural and functional changes to the kidney in diabetic humans and mice.Life sciences · 2013Review
- VEGF and podocytes in diabetic nephropathy.Seminars in nephrology · 2012Review
- New experimental models of diabetic nephropathy in mice models of type 2 diabetes: efforts to replicate human nephropathy.Experimental diabetes research · 2012Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Previous work identified an important role for hyperglycemia in diabetic nephropathy (The Diabetes Control and Complications Trial Research Group. N Engl J Med 329: 977-986, 1993; UK Prospective Diabetes Study Group. Lancet 352: 837-853, 1998), and increased glomerular GLUT1 has been implicated. However, the roles of GLUT1 and intracellular glucose have not been determined. Here, we developed transgenic GLUT1-overexpressing mice (GT1S) to characterize the roles of GLUT1 and intracellular glucose in the development of glomerular disease without diabetes. GLUT1 was overexpressed in glomerular mesangial cells (MC) of C57BL6 mice, a line relatively resistant to diabetic nephropathy. Blood pressure, blood glucose, glomerular morphometry, matrix proteins, cell signaling, transcription factors, and selected growth factors were examined. Kidneys of GT1S mice overexpressed GLUT1 in glomerular MCs and small vessels, rather than renal tubules. GT1S mice were neither diabetic nor hypertensive. Glomerular GLUT1, glucose uptake, mean capillary diameter, and mean glomerular volume were all increased in the GT1S mice. Moderately severe glomerulosclerosis (GS) was established by 26 wk of age in GT1S mice, with increased glomerular type IV collagen and fibronectin. Modest increases in glomerular basement membrane thickness and albuminuria were detected with podocyte foot processes largely preserved, in the absence of podocyte GLUT1 overexpression. Activation of glomerular PKC, along with increased transforming growth factor-beta1, VEGFR1, VEGFR2, and VEGF were all detected in glomeruli of GT1S mice, likely contributing to GS. The transcription factor NF-kappaB was also activated. Overexpression of glomerular GLUT1, mimicking the diabetic GLUT1 response, produced numerous features typical of diabetic glomerular disease, without diabetes or hypertension. This suggested GLUT1 may play an important role in the development of diabetic GS.
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