Document Detail

Increment and impairment of adiponectin in renal failure.
MedLine Citation:
PMID:  20035033     Owner:  NLM     Status:  MEDLINE    
AIMS: Patients with chronic renal failure are at high risk of cardiovascular diseases. Previous studies in healthy population showed that hypoadiponectinemia was associated with high cardiovascular disease risk. However, plasma adiponectin (APN) levels are increased in renal dysfunction. Therefore, the clinical significance of plasma APN level in patients with moderate renal dysfunction is controversial. The aim of this study was to determine the change of plasma APN levels in a mouse model of renal failure and the loss of vasculo-protective function of APN in the presence of high cystatin C levels.
METHODS AND RESULTS: Subtotal (5/6) nephrectomy was performed in APN-knockout (KO) mice and wild-type (WT) mice. The procedure in WT mice resulted in the significant increase of plasma APN and cystatin C levels. The clearance rate of APN was measured by injecting plasma from WT mice into KO mice. The clearance rate was significantly decreased in subtotal nephrectomized KO mice compared with sham-operated KO mice. Adiponectin protein and mRNA levels in adipose tissue were similar to subtotal nephrectomized and sham-operated mice. In cultured endothelial cells, at a high concentration corresponding to renal failure, cystatin C abolished the suppressive effects of APN on tumour necrosis factor alpha-induced expression of monocyte adhesion molecules.
CONCLUSION: Plasma APN increases in chronic renal failure, at least in part due to low clearance rate. High concentrations of cystatin C abolish the vasculo-protective effect of APN.
Noriyuki Komura; Shinji Kihara; Mina Sonoda; Norikazu Maeda; Yoshihiro Tochino; Tohru Funahashi; Iichiro Shimomura
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-12-24
Journal Detail:
Title:  Cardiovascular research     Volume:  86     ISSN:  1755-3245     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-13     Completed Date:  2010-06-03     Revised Date:  2012-04-09    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  471-7     Citation Subset:  IM    
Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan.
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MeSH Terms
Adiponectin / blood,  deficiency,  genetics,  metabolism
Adipose Tissue, White
Biological Markers / blood
Cell Adhesion Molecules / metabolism
Cells, Cultured
Cystatin C / blood,  metabolism
Disease Models, Animal
Endothelial Cells / metabolism
Kidney Failure, Chronic / genetics,  metabolism*
Metabolic Clearance Rate
Mice, Inbred C57BL
Mice, Knockout
RNA, Messenger / metabolism
Recombinant Proteins / metabolism
Time Factors
Tumor Necrosis Factor-alpha / metabolism
Reg. No./Substance:
0/ADIPOQ protein, human; 0/Adiponectin; 0/Adipoq protein, mouse; 0/Biological Markers; 0/CST3 protein, human; 0/Cell Adhesion Molecules; 0/Cst3 protein, mouse; 0/Cystatin C; 0/RNA, Messenger; 0/Recombinant Proteins; 0/Tumor Necrosis Factor-alpha

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