PMID- 10911637
OWN - NLM
STAT- MEDLINE
DCOM- 20001107
LR  - 20200109
IS  - 0896-8608 (Print)
IS  - 0896-8608 (Linking)
VI  - 20 Suppl 2
DP  - 2000
TI  - Effect of high glucose on peritoneal mesothelial cell biology.
PG  - S15-8
AB  - OBJECTIVE: 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. DESIGN: 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. RESULTS: 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. CONCLUSION: 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.
FAU - Ha, H
AU  - Ha H
AD  - Department of Pharmacology, Yonsei University College of Medicine, Seoul, Korea.
FAU - Lee, H B
AU  - Lee HB
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Perit Dial Int
JT  - Peritoneal dialysis international : journal of the International Society for 
      Peritoneal Dialysis
JID - 8904033
RN  - 0 (Chemokine CCL2)
RN  - 0 (Dialysis Solutions)
RN  - 0 (Fibronectins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Transforming Growth Factor beta)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/metabolism
MH  - Dialysis Solutions/toxicity
MH  - Epithelial Cells/*metabolism
MH  - Extracellular Matrix/metabolism
MH  - Fibronectins/genetics/metabolism
MH  - Fibrosis/chemically induced
MH  - Glucose/*pharmacology
MH  - Humans
MH  - Peritoneal Dialysis
MH  - Peritoneum/cytology/*metabolism
MH  - Protein Kinase C/metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Reactive Oxygen Species/metabolism
MH  - Transforming Growth Factor beta/metabolism
MH  - Up-Regulation
RF  - 15
EDAT- 2000/07/27 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/07/27 11:00
PHST- 2000/07/27 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/07/27 11:00 [entrez]
PST - ppublish
SO  - Perit Dial Int. 2000;20 Suppl 2:S15-8.