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This Article Full Text Full Text (PDF) All Versions of this Article: 289/2/F401    most recent 00408.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Morais, C. Articles by Healy, H. Search for Related Content PubMed PubMed Citation Articles by Morais, C. Articles by Healy, H.

High ambient glucose is effect neutral on cell death and proliferation in human proximal tubular epithelial cells

¹Conjoint Renal Laboratory, Queensland Health Pathology Service, Royal Brisbane and Women's Hospital, Bancroft Centre, Brisbane; ²Department of Molecular Cellular Pathology, School of Medicine, University of Queensland, Herston, Brisbane; and ³Department of Renal Medicine, Royal Brisbane and Women's Hospital, Herston, Brisbane, Australia

Submitted 15 November 2004 ; accepted in final form 10 April 2005

In vitro models of diabetic nephropathy that assess the role of hyperglycemia on proximal tubular cell turnover commonly compare cells in a high-glucose medium (25 or 30 mM) with a low-glucose medium (5 to 6.1 mM). Any cellular growth changes observed are usually attributed to the effect of high glucose. We hypothesize that in such experiments, glucose concentrations in the low-glucose medium may decline during the course of the experiments to levels that inhibit cell growth leading to the comparative conclusion that high glucose induces hyperplasia and/or hypertrophy. In this study, primary cultures of human proximal tubular epithelial cells (PTEC) and immortalized HK-2 cells were exposed to low (5 mM) or high (17, 30, or 47 mM) glucose for up to 6 days (PTEC) and 48 h (HK-2). When culture media were not replenished, low glucose induced a significant increase in necrosis and release of lactate dehydrogenase and a decrease in proliferation, metabolic activity, and protein content without any changes in apoptosis. High-glucose media failed to induce any of these changes. Glucose was undetectable in the low-glucose culture medium after 72 h. No significant differences were observed between any of the treatment groups when culture media were replenished daily. We conclude that regular replenishment of culture media is necessary to prevent the emergence of artifactual and misleading differences between high- and low-glucose groups. The current knowledge of the pathophysiology of high glucose based on cell culture systems may need to be reevaluated.

apoptosis; diabetic nephropathy; hyperglycemia; necrosis; proximal tubule

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