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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:2428.)
© 2000 American Heart Association, Inc.

Atherosclerosis and Lipoproteins

Bezafibrate Increases Preß1-HDL at the Expense of HDL_2b in Hypertriglyceridemia

Takashi Miida; Katsuyuki Sakai; Kazuyuki Ozaki; Yuichi Nakamura; Toshio Yamaguchi; Takashi Tsuda; Takayuki Kashiwa; Toru Murakami; Koichi Inano; Masahiko Okada

From the Department of Laboratory Medicine (T. Miida, K.I., M.O.) and the First Department of Internal Medicine (K.S., K.O., Y.N.), Niigata University School of Medicine, Niigata; the Department of Cardiology, Kido Hospital (T.Y., T.T.), Niigata; the Institute of Medical Science, St. Marianna University School of Medicine (T.K.), Kawasaki; and the Department of Pharmaceutical Care and Clinical Pharmacy (T. Murakami), Tokushima Bunri University, Tokushima, Japan.

Correspondence to Takashi Miida, Department of Laboratory Medicine, Niigata University School of Medicine, Asahimachi 1-757, Niigata, Niigata 951-8510, Japan. E-mail miida{at}med.niigata-u.ac.jp

Abstract—Preß1-high density lipoprotein (preß1-HDL), the initial acceptor of cell-derived cholesterol, can be generated from HDL₂ by hepatic lipase. Because bezafibrate elevates lipase activity, it may increase preß1-HDL at the expense of HDL₂. To answer this question, we determined the apolipoprotein A-I (apoA-I) distribution in 20 hypertriglyceridemics (triglycerides>2.26 mmol/L) and 20 sex-matched normolipidemics by native 2-dimensional gel electrophoresis. At baseline, preß1-HDL was 70% higher in hypertriglyceridemics than in normolipidemics (123.5±49.9 versus 72.5±34.1 mg/L apoA-I, P<0.01). Preß1-HDL was positively correlated with triglyceride (r=0.624, P<0.0001). A 4-week bezafibrate treatment (400 mg daily) increased preß1-HDL by 30% (160.2±64.5 mg/L apoA-I, P<0.05) but decreased HDL_2b by 31% (from 188.8±94.9 to 129.3±78.7 mg/L apoA-I, P<0.05). Hepatic lipase activity increased by 24% (P<0.005). Preß1-HDL was generated either from ultracentrifugally isolated HDL₂ or from plasma during incubation with triglyceride lipase. In conclusion, bezafibrate increases preß1-HDL at the expense of HDL₂. We speculate that such an effect might partly contribute to the antiatherogenic action of bezafibrate.

Key Words: pre-ß-HDL • hepatic lipase • apolipoprotein A-I • LpA-I • cholesteryl ester transfer protein

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