Mice lacking acylation stimulating protein (ASP) have delayed postprandial triglyceride clearance. Academic Article uri icon

abstract

  • Acylation stimulating protein (ASP) is a 76 amino acid fragment of the third component of complement (C3) which is generated by the interaction of adipsin and factor B with C3. In vitro studies have shown that ASP can markedly increase triglyceride synthesis in adipocytes. To test the ASP pathway in vivo, C3-deficient mice, and therefore ASP-deficient mice, were generated and oral fat loads were conducted in wild-type (C3+/+) and mutant (C3-/-) animals. The principal results were: 1) postprandial triglyceride clearance was significantly delayed in mutant compared to wild-type mice; 2) this difference was more pronounced in males compared to females; 3) in both males and females, the differences were more pronounced in the second half of the postprandial period; 4) fasting and postprandial free fatty acid (FFA) were higher in C3(-/-) than in C3(+/+) males; and 5) intraperitoneal administration of ASP accelerated triglyceride clearance in C3(-/-) males. The data are consistent therefore, with the hypothesis that the ASP pathway is an important physiologic determinant of normal postprandial triglyceride clearance.

published proceedings

  • J Lipid Res

altmetric score

  • 6

author list (cited authors)

  • Murray, I., Sniderman, A. D., & Cianflone, K.

citation count

  • 60

complete list of authors

  • Murray, I||Sniderman, AD||Cianflone, K

publication date

  • September 1999