Clinical Chemistry
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Clinical Chemistry 55: 2049-2052, 2009. First published August 27, 2009; 10.1373/clinchem.2009.128645
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(Clinical Chemistry. 2009;55:2049-2052.)
© 2009 American Association for Clinical Chemistry, Inc.

Brief Communication

Plasma Proprotein Convertase Subtilisin/Kexin Type 9: A Marker of LDL Apolipoprotein B-100 Catabolism?

Dick C. Chan1, Gilles Lambert2,3, P. Hugh R. Barrett1, Kerry-Anne Rye2,4, Esther M.M. Ooi1 and Gerald F. Watts1,a

1 Metabolic Research Centre, School of Medicine and Pharmacology, University of Western Australia, Perth, Australia; 2 The Heart Research Institute, Sydney, Australia; 3 Université de Nantes, Faculté de Médecine, Nantes, France; 4 Department of Medicine, University of Sydney, Sydney, Australia;

aaddress correspondence to this author at: School of Medicine and Pharmacology, University of Western Australia, Royal Perth Hospital, GPO Box X2213, Perth, WA 6847, Australia. Fax 61-8-92240246; e-mail Gerald.watts{at}uwa.edu.au.


Abstract

Background: Experimental studies suggest that proprotein convertase subtilisin/kexin type 9 (PCSK9) is an important regulator of LDL metabolism because of its ability to facilitate degradation of the LDL receptor. We investigated the association between plasma PCSK9 concentration and LDL apolipoprotein B-100 (apo B-100) metabolism in men with a wide range of body mass index values.

Methods: We used GC-MS to study the kinetics of LDL apo B-100 after intravenous administration of deuterated leucine and analyzed the data by compartmental modeling. The plasma PCSK9 concentration was measured by ELISA.

Results: Univariate regression analysis revealed the plasma PCSK9 concentration to be significantly and positively correlated with cholesterol (r = 0.543; P = 0.011), LDL cholesterol (r = 0.543; P = 0.011), apo B-100 (r = 0.548; P = 0.010), and LDL apo B-100 concentrations (r = 0.514; P = 0.023), and inversely correlated with the LDL apo B-100 fractional catabolic rate (FCR) (r = –0.456; P = 0.038). The association between plasma PCSK9 concentration and the LDL apo B-100 FCR remained statistically significant after adjusting for age, obesity, plasma insulin, homeostasis model assessment score, and dietary energy; however, this association had borderline significance after adjusting for plasma lathosterol.

Conclusions: In men, variation in plasma PCSK9 concentration influences the catabolism of LDL apo B-100. This finding appears to be independent of obesity, insulin resistance, energy intake, and age.






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Copyright © 2009 by the American Association for Clinical Chemistry.