Lipoprotein lipase and hepatic lipase: Their relationship with HDL subspecies Lp(A-I) and Lp(A-I,A-II)

Marian C. Cheung, Shalamar D. Sibley, Jerry P. Palmer, John F. Oram, and John D. Brunzell

Department of Medicine, University of Washington, Seattle, WA 98103

Corresponding Author: mccheung{at}u.washington.edu

Existing evidence suggests that human high density lipoprotein (HDL) particles containing apolipoprotein (apo) A-I with or without apoA-II [Lp(A-I) and Lp(A-I,A-II)] have different anti-atherogenic potentials. To determine the role of lipoprotein lipase (LPL) and hepatic lipase (HL) in regulating these particles in vivo, we measured the activities of these enzymes in the post-heparin plasma of 28 healthy subjects with well-controlled type 1 diabetes, and studied their relationship with Lp(A-I) and Lp(A-I,A-II). LPL was positively correlated with the apoA-I, cholesterol, and phospholipid mass in total Lp(A-I), and with the apoA-I mass in large Lp(A-I) (r > 0.58, p < 0.001). HL was negatively correlated with all the above Lp(A-I) parameters plus Lp(A-I) triglyceride (r >-0.53, p < 0.003). No correlation was detected between LPL and Lp(A-I,A-II). However, HL was inversely correlated with the phospholipid in total Lp(A-I,A-II), and with the amounts of large Lp(A-I,A-II) (r>0.50, p<0.006). Phospholipid transfer protein (PLTP) activity was measured in pre-heparin plasma. Only total Lp(A-I) triglyceride in women (r=0.71, p=0.009) but not in men was significantly correlated with PLTP activity. These observations indicate that LPL and HL play major roles in determining the level and composition of plasma Lp(A-I), particularly large Lp(A-I) particles. In contrast, neither appeared to be major determinants of the amounts of apoA-I and A-II in Lp(A-I,A-II). Furthermore, significant correlations of LPL and/or HL with the apoA-I, cholesterol, and triglyceride of Lp(A-I) but not Lp(A-I,A-II) imply that the apoA-I and lipid of Lp(A-I) and Lp(A-I,A-II) are not fully equilibrated.

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