ArticleAmerican journal of physiology. Renal physiology2010
Podocyte-specific overexpression of GLUT1 surprisingly reduces mesangial matrix expansion in diabetic nephropathy in mice.
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 25 papers.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- Food-grade nanostructured delivery systems for oral administration of astaxanthin: Bioprocessing strategies and therapeutic applications.NPJ science of food · 2025Review
- Astaxanthin-Based Biomaterials for Tissue Repair and Drug Delivery Systems.Biomaterials research · 2025Review
- Targeted drug delivery strategy: a bridge to the therapy of diabetic kidney disease.Drug delivery · 2023Article
- Diabetic vascular diseases: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2023Review
- Nanotechnology-Abetted Astaxanthin Formulations in Multimodel Therapeutic and Biomedical Applications.Journal of medicinal chemistry · 2022Review
- Gene expression profiles of diabetic kidney disease and neuropathy in eNOS knockout mice: Predictors of pathology and RAS blockade effects.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Lipid mediators of insulin signaling in diabetic kidney disease.American journal of physiology. Renal physiology · 2019Review
- Ion channels and transporters in diabetic kidney disease.Current topics in membranes · 2019Review
- Role of Podocyte Injury in Glomerulosclerosis.Advances in experimental medicine and biology · 2019Review
- Assessment of Kidney Function in Mouse Models of Glomerular Disease.Journal of visualized experiments : JoVE · 2018Article
- 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
- The Evolving Importance of Insulin Signaling in Podocyte Health and Disease.Frontiers in endocrinology · 2018Review
- Podocyte-specific JAK2 overexpression worsens diabetic kidney disease in mice.Kidney international · 2017Article
- Canonical Transient Receptor Potential 6 Channel: A New Target of Reactive Oxygen Species in Renal Physiology and Pathology.Antioxidants & redox signaling · 2016Review
- Low-Dose IL-17 Therapy Prevents and Reverses Diabetic Nephropathy, Metabolic Syndrome, and Associated Organ Fibrosis.Journal of the American Society of Nephrology : JASN · 2016Article
- Article
- Deletion of UNC5B in Kidney Epithelium Exacerbates Diabetic Nephropathy in Mice.American journal of nephrology · 2015Article
- Insulin signaling: implications for podocyte biology in diabetic kidney disease.Current opinion in nephrology and hypertension · 2015Article
- Urinary semaphorin 3A correlates with diabetic proteinuria and mediates diabetic nephropathy and associated inflammation in mice.Journal of molecular medicine (Berlin, Germany) · 2014Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Increased expression of the facilitative glucose transporter, GLUT1, leads to glomerulopathy that resembles diabetic nephropathy, whereas prevention of enhanced GLUT1 expression retards nephropathy. While many of the GLUT1-mediated effects are likely due to mesangial cell effects, we hypothesized that increased GLUT1 expression in podocytes also contributes to the progression of diabetic nephropathy. Therefore, we generated two podocyte-specific GLUT1 transgenic mouse lines (driven by a podocin promoter) on a db/m C57BLKS background. Progeny of the two founders were used to generate diabetic db/db and control db/m littermate mice. Immunoblots of glomerular lysates showed that transgenic mice had a 3.5-fold (line 1) and 2.1-fold (line 2) increase in GLUT1 content compared with wild-type mice. Both lines showed similar increases in fasting blood glucose and body weights at 24 wk of age compared with wild-type mice. Mesangial index (percent PAS-positive material in the mesangial tuft) increased 88% (line 1) and 75% (line 2) in the wild-type diabetic mice but only 48% (line 1) and 39% (line 2) in the diabetic transgenic mice (P < 0.05, transgenic vs. wild-type mice). This reduction in mesangial expansion was accompanied by a reduction in fibronectin accumulation, and vascular endothelial growth factor (VEGF) levels increased only half as much in the transgenic diabetic mice as in wild-type diabetic mice. Levels of nephrin, neph1, CD2AP, podocin, and GLUT4 were not significantly different in transgenic compared with wild-type mice. Taken together, increased podocyte GLUT1 expression in diabetic mice does not contribute to early diabetic nephropathy; surprisingly, it protects against mesangial expansion and fibronectin accumulation possibly by blunting podocyte VEGF increases.
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