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Adipsin and an endogenous pathway of complement from adipose cells
L N Choy1, B S Rosen, B M Spiegelman
1Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115.
The Journal of Biological Chemistry
|June 25, 1992
Summary
Adipose tissue activates the alternative complement pathway, producing biologically active molecules. This localized complement activation is impaired in obese mice, suggesting a role in energy balance.
Area of Science:
- Immunology
- Metabolic Research
- Adipose Tissue Biology
Background:
- The alternative complement pathway is crucial for immune responses against pathogens.
- Adipose cells synthesize adipsin (complement factor D homolog), with reduced levels in obesity.
- The role of adipose tissue in complement activation is not fully understood.
Purpose of the Study:
- To investigate the synthesis and activation of alternative complement pathway components by adipose cells and tissue.
- To determine if adipose tissue can activate the proximal alternative complement pathway independently of infection.
- To examine the impact of obesity on localized complement activation in adipose tissue.
Main Methods:
- In vitro synthesis of complement factors C3 and B by cultured adipocytes and adipose tissue explants.
- Detection of complement activation products, including anaphylatoxin C3a.
- Comparison of complement activation in adipose tissue from lean and obese mice.
Main Results:
- Adipose cells and tissue synthesize complement factors C3 and B.
- Adipose tissue activates the proximal alternative complement pathway, producing bioactive polypeptides like C3a.
- This activation occurs without triggering the terminal lytic pathway and is impaired in obese mice.
- Cultured adipocytes require cytokine stimulation, while adipose tissue explants do not.
Conclusions:
- Adipose tissue represents a localized site for alternative complement pathway activation.
- This pathway activation in adipose tissue is linked to metabolic state and potentially energy balance.
- Impaired complement activation in obesity suggests a novel role in metabolic dysfunction.