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This Article Full Text Full Text (PDF) All Versions of this Article: 294/3/E521    most recent 00590.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Paglialunga, S. Articles by Cianflone, K. Search for Related Content PubMed PubMed Citation Articles by Paglialunga, S. Articles by Cianflone, K.

Acylation-stimulating protein deficiency and altered adipose tissue in alternative complement pathway knockout mice

¹Department of Biochemistry, McGill University, Montreal; ²Centre de Recherche de l'Hôpital Laval, Université Laval, Québec, Canada; and ³Institute of Biomedicine, Sahlgrenska Academy at Göteborg University, Gothenberg, Sweden

Submitted 10 September 2007 ; accepted in final form 21 December 2007

Acylation-stimulating protein (C3adesArg/ASP) is an adipokine that acts on its receptor C5L2 to stimulate triglyceride (TG) synthesis in adipose tissue. The present study investigated ASP levels in mouse models of obesity and leanness and the effect of ASP deficiency in C3 knockout (C3KO) mice on adipose tissue morphology. Plasma ASP levels in wild-type (WT) mice correlated positively with plasma nonesterified fatty acids (NEFA) (R = 0.664, P < 0.001) and total cholesterol (R = 0.515, P < 0.001). Plasma ASP was increased by 85% in obese ob/ob leptin-deficient mice and decreased in lean diacylglycerol acyltransferase 1 (DGAT1) KO mice (–54%) and C/EBP^β/β transgenic mice (–70%) compared with WT. Mice lacking alternative complement factor B or adipsin (FBKO or ADKO), required for ASP production, were also ASP deficient. Both FBKO and C3KO mice had delayed postprandial TG and NEFA clearance on low-fat (LF) and high-fat (HF) diets, suggesting that lack of ASP, not C3, drives the metabolic phenotype. Adipocyte size distribution in C3KO mice was polarized (increased number of both small and large cells), with decreased adipsin expression (–33% gonadal HF), DGAT1 expression (–31% to –50%) and DGAT activity (–41%). Overall, a reduction/deficiency in ASP is associated with an antiadipogenic state and ASP may provide a target for controlling fat storage.

C3adesArg; complement C3; factor B; diacylglycerol acyltransferase 1; postprandial lipemia

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