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Alterations of the Classic Pathway of Complement in Adipose Tissue of Obesity and Insulin Resistance.

Authors: Zhang, J  Wright, W  Bernlohr, DA  Cushman, SW  Chen, X 
Citation: Zhang J, etal., Am J Physiol Endocrinol Metab. 2007 Jan 23;.
Pubmed: (View Article at PubMed) PMID:17244723
DOI: Full-text: DOI:10.1152/ajpendo.00664.2006

Adipose tissue inflammation has been recently linked to the pathogenesis of obesity and insulin resistance. C1 complex comprising three distinct proteins C1q, C1r, and C1s involves the key initial activation of the classic pathway of complement and plays an important role in the initiation of inflammatory process. In this study, we investigated adipose expression and regulation of C1 complement subcomponents and C1 activation regulator decorin in obesity and insulin resistance. Expression of C1q in epididymal adipose tissue was increased consistently in ob/ob mice, Zucker obese rats and high fat diet-induced obese (HF-DIO) mice. Decorin was found to increase in expression in Zucker obese rats and HF-DIO mice, but decrease in ob/ob mice. After TZD administration, C1q and decorin expression was reversed in Zucker obese rats and HF-DIO mice. Increased expression of C1 complement and decorin was observed in both primary adipose and S-V cells isolated from Zucker obese rats. Up-regulation of C1r and C1s expression was also perceived in adipose cells from insulin resistant humans. Further, expression of C1 complement and decorin is dysregulated in TNF α-induced insulin resistance in 3T3-L1 adipocytes and cultured rat adipose cells as they became insulin resistant after 24h culture. This data suggests that both adipose and immune cells are the sources for abnormal adipose tissue production of C1 complement and decorin in obesity. Our findings also demonstrate that excessive activation of the classic pathway of complement commonly occurs in obesity, suggesting its possible role in adipose tissue inflammation and insulin resistance. Key words: C1 complement, adipose, insulin resistance, obesity, gene expression.


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RGD Object Information
RGD ID: 1600551
Created: 2007-03-13
Species: All species
Last Modified: 2007-03-13
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.