Complement 3 (C3) through its interaction with factors B and D (adipsin) generates C3a. In the human body, C3a is rapidly cleaved by carboxypeptidase B or carbxyopeptidase N, that remove the carboxyl-terminal arginine to generate C3adesArg.[1] Thus, most of plasmatic C3a is present in C3adesArg form. C3adesArg is more commonly named ASP or acylation-stimulating-protein due to its marked stimulating action on triacylglycerol synthesis in human adipocytes and skin fibroblasts.[2] ASP is also known for its augmentation of glucose transport and inhibiting action on hormone-sensitive lipase. Because of these actions, it is linked to the pathogenesis of obesity,[3] having been demonstrated to be present at increased levels in patients with obesity,[4] diabetes mellitus type 2[5] and coronary artery disease.[6]

ASP lis a ligand for C5L2, a G-protein-coupled receptor.[7]

The view of C3a/C3adesArg as an acylation stimulating activity is not universally accepted. The evidence is discussed in a recent review.[8]

References

  1. ↑ Baldo et al. 1993, pp. 1543–1547
  2. ↑ Cianflone et al., pp. 426–430
  3. ↑ (Sniderman, Maslowska & Cianflone 2000, pp. 291–296)
  4. ↑ Maslowska et al. 1999, pp. 679–686
  5. ↑ Koistinen et al. 2001, pp. 1034–1039
  6. ↑ Cianflone et al. 1997, pp. 1239–1244
  7. ↑ Cui et al. 2009, pp. 3207–3217
  8. ↑ Klos A, Wende E, Wareham KJ, Monk PN (2013). "International Union of Pharmacology. LXXXVII. Complement peptide C5a, C4a, and C3a receptors". Pharmacol. Rev. 65 (1): 500–43. doi:10.1124/pr.111.005223. PMID 23383423.

Further reading

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