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Quantitative Determination of De Novo Fatty Acid Synthesis in Brown Adipose Tissue Using Deuterium Oxide
Published on: May 12, 2023
A new effector of lipid metabolism: complement factor properdin.
Danny Gauvreau1, Christian Roy, Fun-Qun Tom
1Institut Universitaire de Cardiologie et de Pneumologie de Quebec Research Center, Quebec, QC, Canada.
Molecular Immunology
|March 6, 2012
Summary
Properdin deficiency in mice leads to increased weight gain and altered lipid metabolism, suggesting a role for properdin in energy balance and adipose tissue function.
Area of Science:
- Immunology
- Metabolic Research
- Adipose Tissue Biology
Background:
- The complement system, crucial for innate immunity, is increasingly recognized for its roles in adipose tissue.
- Properdin, a complement activator, stabilizes C3 convertase and is found on adipocyte membranes.
Purpose of the Study:
- To investigate the role of properdin in energy metabolism.
- To utilize properdin-deficient (PKO) mice and cell-based assays for this evaluation.
Main Methods:
- Comparison of PKO mice with wild-type (WT) littermates on high-fat diets.
- Assessment of weight gain, body fat mass, energy expenditure, and postprandial lipid clearance.
- In vitro studies using 3T3-L1 adipocytes and L6 rat skeletal muscle cells to examine properdin's effects on glucose and lipid metabolism.
Main Results:
- PKO mice exhibited diet-dependent weight gain and increased fat mass on a high-fat diet.
- Decreased energy expenditure and altered lipid clearance were observed in PKO mice.
- Properdin inhibited insulin-mediated fatty acid uptake in adipocytes but did not affect glucose transport.
Conclusions:
- Properdin influences lipid metabolism and energy storage in adipose tissue.
- This finding supports a dual role for complement proteins in regulating adipose tissue function and potentially insulin resistance.
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