Acylation stimulating protein

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Complement 3 (C3) through its interaction with factors B and D (adipsin) generates C3a. In the human body, C3a is rapidily 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 ligates a specific receptor named C5L2 which is coupled with a G-protein.[7]

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


  1. ^ (Baldo et al. 1993, pp. 1543–1547)
  2. ^ (Cianflone, Sniderman & Walsh Vu1989, 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. 

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