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      Effect of high glucose on peritoneal mesothelial cell biology.

      Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis

      Animals, Up-Regulation, metabolism, Transforming Growth Factor beta, Reactive Oxygen Species, Rats, RNA, Messenger, Protein Kinase C, cytology, Peritoneum, Peritoneal Dialysis, Humans, pharmacology, Glucose, chemically induced, Fibrosis, genetics, Fibronectins, Extracellular Matrix, Epithelial Cells, toxicity, Dialysis Solutions, Chemokine CCL2

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          This study reviews evidence that implicates high glucose (HG) in the pathogenesis of peritoneal fibrosis and proposes mechanisms potentially involved in the HG-induced peritoneal fibrosis that is observed in long-term peritoneal dialysis (PD) patients. Selected Western literature is reviewed, examining the effect of HG on rat or human peritoneal mesothelial cell (HPMC) biology with particular reference to extracellular matrix (ECM) gene expression and protein synthesis. HG up-regulated the expression of monocyte chemotactic peptide-1 (MCP-1), transforming growth factor beta 1 (TGF beta 1), and fibronectin messenger RNAs (mRNAs) and proteins. These HG-induced up-regulations were effectively blocked by the inhibition of protein kinase C (PKC). In addition, cytosolic reactive oxygen species (ROS) rapidly increased in HPMC cultured under HG, and treatment with antioxidant effectively inhibited HG-induced fibronectin protein synthesis by HPMC. Continuous exposure of the peritoneal membrane to HG may induce changes in HPMC biology, leading to excessive deposition of ECM and peritoneal injury. HG-induced activation of diacylglycerol PKC (DAG-PKC) plays a major role in up-regulation of MCP-1, TGF beta 1, and fibronectin synthesis by HPMC cultured under HG. In addition, ROS, recently recognized as signalling molecules, are rapidly generated in HPMC as a result of increased glucose metabolism and may prove to be an important mediator of HG-induced peritoneal injury.

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