Of mice and men (and women) and the acylation-stimulating protein pathway

Curr Opin Lipidol. 2000 Jun;11(3):291-6. doi: 10.1097/00041433-200006000-00010.


The storage and release of energy by adipocytes is of fundamental biologic importance. Not surprisingly, therefore, the rate at which these processes occur can be modulated by a variety of physiologic molecules. A newly recognized participant is produced by adipocytes themselves: acylation-stimulating protein (ASP). This article focuses on the most recent in-vivo evidence regarding how the ASP pathway may influence energy storage and release. In brief, the rate at which triglycerides are cleared from plasma (i.e. the rate at which they are hydrolysed) is determined by lipoprotein lipase and insulin, which is the principal hormone that regulates lipoprotein lipase. By contrast, the ASP pathway modulates the rate at which fatty acids are taken up and converted to triglycerides by adipocytes. Under certain circumstances, however, reduction of activity of the ASP pathway may negatively impact on the first step of the process. ASP also influences the rate at which fatty acids are released by adipocytes, and it is clear that insulin and ASP interact in a variety of ways that involve energy storage and release. Accordingly, to understand the impact of any intervention on energy storage and release by adipocytes, the effects of both insulin and ASP must be taken into account.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adipocytes / metabolism
  • Animals
  • Apolipoproteins B / genetics
  • Apolipoproteins B / metabolism*
  • Blood Proteins / genetics
  • Blood Proteins / metabolism*
  • Complement C3a* / analogs & derivatives*
  • Fatty Acids / metabolism
  • Female
  • Humans
  • Insulin Resistance
  • Male
  • Mice
  • Mice, Knockout
  • Triglycerides / blood


  • Apolipoproteins B
  • Blood Proteins
  • Fatty Acids
  • Triglycerides
  • complement C3a, des-Arg-(77)-
  • Complement C3a