In this installment, we reunite with our old friend C3KO mouse to learn a little bit more about the role of acylation stimulating protein, ASP, in the regulation of fat tissue (and muscle) from this study:
Differential regulation of fatty acid trapping in mouse adipose tissue and muscle by ASP. The C3KO mouse was discussed in
Part II of this series. This mouse lacks the gene to produce a protein called C3 (short for Complement 3) which is a precursor for the formation of ASP. Thus C3KO mice are ASP deficient. The C3KO is to ASP as a type1 diabetic is to insulin. These mice are also resistant to obesity. BTW, hyperASPemia accompanies the hyperinsulinemia and hyperleptinemia of obesity when it's measured.
ASP-deficient mice have delayed postprandial triglyceride (TG) clearance and reduced WAT mass. The objective of this study was to examine the mechanism(s) by which ASP deficiency induces differences in postprandial TG clearance and body composition in male KO mice.
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