ArticleThe Journal of clinical investigation1996
D-glucose-induced dysmorphogenesis of embryonic kidney.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 62 citations in OpenAlex.
- Associations between maternal chronic diseases and congenital anomalies of the kidney and urinary tract in offspring: a population-based cohort study.Clinical kidney journal · 2023Article
- Effects of Environmental Conditions on Nephron Number: Modeling Maternal Disease and Epigenetic Regulation in Renal Development.International journal of molecular sciences · 2021Article
- In utero exposure to maternal diabetes impairs nephron progenitor differentiation.American journal of physiology. Renal physiology · 2019Article
- Inducible ATF3-NFAT axis aggravates podocyte injury.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Concepts for a therapeutic prolongation of nephrogenesis in preterm and low-birth-weight babies must correspond to structural-functional properties in the nephrogenic zone.Molecular and cellular pediatrics · 2017Review
- Special Morphological Features at the Interface of the Renal Stem/Progenitor Cell Niche Force to Reinvestigate Transport of Morphogens During Nephron Induction.BioResearch open access · 2016Review
- Anti-TGF-β Antibody, 1D11, Ameliorates Glomerular Fibrosis in Mouse Models after the Onset of Proteinuria.PloS one · 2016Article
- Altered ureteric branching morphogenesis and nephron endowment in offspring of diabetic and insulin-treated pregnancy.PloS one · 2013Article
- Gestational diabetes affects postnatal development of transport and enzyme functions in rat intestine.Molecular and cellular biochemistry · 2012Article
- AMP-activated protein kinase (AMPK) negatively regulates Nox4-dependent activation of p53 and epithelial cell apoptosis in diabetes.The Journal of biological chemistry · 2010Article
- p66Shc mediates high-glucose and angiotensin II-induced oxidative stress renal tubular injury via mitochondrial-dependent apoptotic pathway.American journal of physiology. Renal physiology · 2010Article
- A comparative proteomic study of nephrogenesis in intrauterine growth restriction.Pediatric nephrology (Berlin, Germany) · 2010Article
- Mechanisms of podocyte injury in diabetes: role of cytochrome P450 and NADPH oxidases.Diabetes · 2009Article
- Effects of early postnatal hyperglycaemia on renal cortex maturity, endothelial nitric oxide synthase expression and nephron deficit in mice.International journal of experimental pathology · 2008Article
- Amelioration of progressive renal injury by genetic manipulation of Klotho gene.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Hyperglycemia: its imminent effects on mammalian nephrogenesis.Pediatric nephrology (Berlin, Germany) · 2005Review
- Neph1 and nephrin interaction in the slit diaphragm is an important determinant of glomerular permeability.The Journal of clinical investigation · 2003Article
- Delayed catabolism of apoB-48 lipoproteins due to decreased heparan sulfate proteoglycan production in diabetic mice.The Journal of clinical investigation · 2000Article
- Diabetes induces changes in glomerular development and laminin-beta 2 (s-laminin) expression.The American journal of pathology · 1997Article
- Developmental regulation and the role of insulin and insulin receptor in metanephrogenesis.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
An organ culture system was used to study the effect of D-glucose on embryonic kidneys, and to delineate the mechanism(s) relevant to their dysmorphogenesis. Metanephroi were cultured in the presence of 30 mM D-glucose. A notable reduction in the size and population of nephrons was observed. Ureteric bud branches were rudimentary and the acuteness of their tips, the site of nascent nephron formation, was lost. Metanephric mesenchyme was atrophic, had reduced cell replication, and contained numerous apoptotic cells. Competitive reverse transcriptase-PCR analyses and immunoprecipitation studies indicated a decrease in expression of heparan sulfate proteoglycan (perlecan). Status of activated protein-2 was evaluated since its binding motifs are present in the promoter region of the perlecan gene. Decreased binding activity of activated protein-2, related to its phosphorylation, was observed. D-glucose-treated explants also had reduced levels of cellular ATP. Exogenous administration of ATP restored the altered metanephric morphology and reduced [35S]sulfate-incorporated radioactivity associated with perlecan. The data suggest that D-glucose adversely affects the metanephrogenesis by perturbing various cellular phosphorylation events involved in the transcriptional and translational regulation of perlecan. Since perlecan modulates epithelial/mesenchymal interactions, its deficiency may have led to the metanephric dysmorphogenesis and consequential atrophy of the mesenchyme exhibiting accelerated apoptosis.
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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 OpenQuestion graph.