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Journal of Lipid Research, Vol. 50, 1109-1119, June 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Lipoprotein lipase deficiency is associated with elevated acylation stimulating protein plasma levels

Sabina Paglialunga^*,, Pierre Julien, Youssef Tahiri^*, Francois Cadelis, Jean Bergeron, Daniel Gaudet^** and Katherine Cianflone^1,*,

^* Biochemistry Department and Faculty of Medicine, McGill University, Montreal, QC, Canada
Centre de Recherche Hôpital Laval, Université Laval, Québec, QC, Canada
Lipid Research Center, Centre Hospitalier Universitaire de Québec (CHUQ) Research Center, Québec, QC, Canada
^** Université de Montréal and Community Genomic Medicine Center Lipid Clinic, Chicoutimi Hospital, Chicoutimi, Québec, QC, Canada

This study was supported by a grant from the Canadian Institute of Health Research (MOP-77532 to K.C.) and the Heart and Stroke Foundation of Quebec (P.J.). K.C. holds a Canada Research Chair in Adipose Tissue.

Published, JLR Papers in Press, February 23, 2009.

¹ To whom correspondence should be addressed. e-mail: Katherine.cianflone{at}crhl.ulaval.ca

Acylation stimulating protein (ASP, C3adesArg) is an adipose tissue derived hormone that stimulates triglyceride (TG) synthesis. ASP stimulates lipoprotein lipase (LPL) activity by relieving feedback inhibition caused by fatty acids (FA). The present study examines plasma ASP and lipids in male and female LPL-deficient subjects primarily with the P207L mutation, common in the population of Quebec, Canada. We evaluated the fasting and postprandial states of LPL heterozygotes and fasting levels in LPL homozygotes. Homozygotes displayed increased ASP (58–175% increase, P < 0.05–0.01), reduced HDL-cholesterol (64–75% decrease, P < 0.0001), and elevated levels of TG (19–38-fold, P < 0.0001) versus control (CTL) subjects. LPL heterozygotes with normal fasting TG (1.3–1.9 mmol/l) displayed increased ASP (101–137% increase, P < 0.05–0.01) and delayed TG clearance after a fatload; glucose levels remained similar to controls. Hypertriglyceridemics with no known LPL mutation also had increased ASP levels (63–192% increase, P < 0.001). High-TG LPL heterozygotes were administered a fatload before and after fibrate treatment. The treatment reduced fasting and postprandial plasma ASP, TG, and FA levels without changing insulin or glucose levels. ASP enhances adipose tissue fatty-acid trapping following a meal; however in LPL deficiency, high ASP levels are coupled with delayed lipid clearance.

Abbreviations: Apo, apolipoprotein; ASP, acylation stimulating protein; AUC, area under the curve; BMI, body mass index; CTL, control; DGAT, diacylglycerol acyltransferase; high-TG, hypertriglyceridemic; FA, fatty acid; LPL, lipoprotein lipase; NEFA, nonesterified fatty acid; normo-TG, normotriglyceridemic; TG, triglyceride

Supplementary key words C3adesArg • chylomicron • postprandial lipemia • fenofibrate

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