ArticleDiabetologia2007
Renal carcinogenesis in models of diabetes in rats: metabolic changes are closely related to neoplastic development.
Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 31 citations in OpenAlex.
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- Proceedings of the 2025 Division of Translational Toxicology Satellite Symposium.Toxicologic pathology · 2026Article
- Ferulic acid lipid nano capsules versus its native form in alleviating diabetic nephropathy induced in rats through TGF-β1/Hippo pathway crosstalk modulation.Scientific reports · 2025Article
- Knockout of the Carbohydrate Responsive Element Binding Protein Enhances Proliferation and Tumorigenesis in Renal Tubules of Mice.International journal of molecular sciences · 2024Article
- The Influence of Soy Isoflavones and Soy Isoflavones with Inulin on Kidney Morphology, Fatty Acids, and Associated Parameters in Rats with and without Induced Diabetes Type 2.International journal of molecular sciences · 2024Article
- 50 week ultrasound imaging and ultrastructural abnormalities of bladder after sugar diuresis and diabetes mellitus in rats.International urology and nephrology · 2021Article
- Review
- Choosing The Right Animal Model for Renal Cancer Research.Translational oncology · 2020Review
- Arsenic exposure intensifies glycogen nephrosis in diabetic rats.Environmental science and pollution research international · 2019Article
- Glycemic index, glycemic load and carbohydrate intake in association with risk of renal cell carcinoma.Carcinogenesis · 2017Article
- Article
- PI3K/AKT/mTOR pathway plays a major pathogenetic role in glycogen accumulation and tumor development in renal distal tubules of rats and men.Oncotarget · 2015Article
- Over-expression of muscle glycogen synthase in human diabetic nephropathy.Histochemistry and cell biology · 2015Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThere is an increased risk of renal cell carcinoma (RCC) in human diabetes mellitus. We therefore examined the influence of hyperglycaemia and glucose-lowering treatment on nephrocarcinogenesis in rats.
methodsRats (n = 850), which were either spontaneously diabetic, streptozotocin-diabetic or normoglycaemic, were examined with special reference to Armanni-Ebstein lesions (AEL).
resultsIrrespective of the cause of diabetes, diabetic but not normoglycaemic rats developed typical glycogenotic clear-cell AEL. AEL showed strong proliferative activity, which was nearly completely inhibited by EGF receptor blockade (Gefitinib treatment). Many findings suggested a stepwise development of RCCs from AEL. Whereas the number and size of RCCs gradually increased in all diabetic groups, beginning at 6 months after onset of diabetes, normoglycaemic controls did not developed RCC. After 28 months, up to 82% of diabetic animals had at least one RCC. In contrast to the proximal tubules, the distal tubular system, including glycogenotic AEL, had the same levels of enzyme activities as RCC (e.g. high glycogen phosphorylase and synthase activity, lack of glucose 6-phosphatase activity) and the same expression patterns of cytokeratin 7 and several growth factors, along with their receptors and signal transduction proteins (TGF-alpha, EGF receptor, IGF-I, IGF-I receptor, IGF-II receptor, insulin receptor substrate 1, v-raf-1 murine leukemia viral oncogene homologue 1 and mitogen activated protein kinase kinase 1). In addition, direct morphological transitions between distal tubules, AEL and RCCs were frequently observed. All these findings indicate a common origin and a precursor-product relationship of AEL and RCCs. CONCLUSIONS/
interpretationNephrocarcinogenesis in diabetic rats results from sustained hyperglycaemia, resulting in an adaptive metabolic response, altered growth factor signalling and subsequent neoplastic transformation of the tubular epithelial cells.
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