
Bezafibrate Increases Preβ1-HDL at the Expense of HDL 2b in Hypertriglyceridemia
Author(s) -
Takashi Miida,
Katsuyuki Sakai,
Kazuyuki Ozaki,
Yūichi Nakamura,
Tomohiro Yamaguchi,
Takashi Tsuda,
Takayuki Kashiwa,
Toru Murakami,
Koichi Inano,
Masahiko Okada
Publication year - 2000
Publication title -
arteriosclerosis, thrombosis, and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/01.atv.20.11.2428
Subject(s) - bezafibrate , medicine , endocrinology , triglyceride , hypertriglyceridemia , hepatic lipase , lipase , chemistry , lipoprotein lipase , apolipoprotein b , high density lipoprotein , cholesterol , enzyme , biochemistry , adipose tissue
—Preβ1-high density lipoprotein (preβ1-HDL), the initial acceptor of cell-derived cholesterol, can be generated from HDL2 by hepatic lipase. Because bezafibrate elevates lipase activity, it may increase preβ1-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, preβ1-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). Preβ1-HDL was positively correlated with triglyceride (r =0.624,P <0.0001). A 4-week bezafibrate treatment (400 mg daily) increased preβ1-HDL by 30% (160.2±64.5 mg/L apoA-I,P <0.05) but decreased HDL2b 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). Preβ1-HDL was generated either from ultracentrifugally isolated HDL2 or from plasma during incubation with triglyceride lipase. In conclusion, bezafibrate increases preβ1-HDL at the expense of HDL2 . We speculate that such an effect might partly contribute to the antiatherogenic action of bezafibrate.