Lipoprotein lipase deficiency is associated with elevated acylation stimulating protein plasma levels
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...
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Elsevier
2009-06-01
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Series: | Journal of Lipid Research |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S0022227520308099 |
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author | Sabina Paglialunga Pierre Julien Youssef Tahiri Francois Cadelis Jean Bergeron Daniel Gaudet Katherine Cianflone |
author_facet | Sabina Paglialunga Pierre Julien Youssef Tahiri Francois Cadelis Jean Bergeron Daniel Gaudet Katherine Cianflone |
author_sort | Sabina Paglialunga |
collection | DOAJ |
description | 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. |
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spelling | doaj.art-e9a2986ab926469aa99ac8a81c738e8f2022-12-21T20:08:07ZengElsevierJournal of Lipid Research0022-22752009-06-0150611091119Lipoprotein lipase deficiency is associated with elevated acylation stimulating protein plasma levelsSabina Paglialunga0Pierre Julien1Youssef Tahiri2Francois Cadelis3Jean Bergeron4Daniel Gaudet5Katherine Cianflone6Biochemistry 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, CanadaBiochemistry 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, CanadaBiochemistry 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, CanadaBiochemistry 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, CanadaBiochemistry 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, CanadaBiochemistry 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, CanadaBiochemistry 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, CanadaAcylation 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.http://www.sciencedirect.com/science/article/pii/S0022227520308099C3adesArgchylomicronpostprandial lipemiafenofibrate |
spellingShingle | Sabina Paglialunga Pierre Julien Youssef Tahiri Francois Cadelis Jean Bergeron Daniel Gaudet Katherine Cianflone Lipoprotein lipase deficiency is associated with elevated acylation stimulating protein plasma levels Journal of Lipid Research C3adesArg chylomicron postprandial lipemia fenofibrate |
title | Lipoprotein lipase deficiency is associated with elevated acylation stimulating protein plasma levels |
title_full | Lipoprotein lipase deficiency is associated with elevated acylation stimulating protein plasma levels |
title_fullStr | Lipoprotein lipase deficiency is associated with elevated acylation stimulating protein plasma levels |
title_full_unstemmed | Lipoprotein lipase deficiency is associated with elevated acylation stimulating protein plasma levels |
title_short | Lipoprotein lipase deficiency is associated with elevated acylation stimulating protein plasma levels |
title_sort | lipoprotein lipase deficiency is associated with elevated acylation stimulating protein plasma levels |
topic | C3adesArg chylomicron postprandial lipemia fenofibrate |
url | http://www.sciencedirect.com/science/article/pii/S0022227520308099 |
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