Adipsin and complement factor D activity: an immune-related defect in obesity

Area of Science:

• Biochemistry
• Immunology
• Metabolism

Background:

• Adipsin, a serine protease from adipocytes, is deficient in obesity models.
• Defective gene expression is linked to obesity.
• The function of adipsin remains largely unelucidated.

Purpose of the Study:

• To purify and characterize recombinant mouse adipsin.
• To elucidate the biochemical and enzymatic properties of adipsin.
• To investigate the role of adipsin in complement activation and energy balance.

Main Methods:

• Purification of recombinant mouse adipsin.
• Biochemical and enzymatic assays to determine adipsin activity.
• Assessment of complement alternative pathway activation and red blood cell lysis.
• Comparison of adipsin activity in various obesity models.

Main Results:

• Activated adipsin exhibits complement factor D-like activity, cleaving complement factor B.
• Adipsin activates the alternative pathway of complement, leading to red blood cell lysis.
• Significantly decreased complement factor D activity (58-80%) was observed in multiple obesity models (ob/ob, db/db, MSG-injected mice, fa/fa rats).

Conclusions:

• Adipsin functions analogously to complement factor D.
• Adipsin activates the complement alternative pathway.
• Adipsin and the complement alternative pathway may play a crucial role in regulating systemic energy balance.