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Volume 272, Number 21, Issue of May 23, 1997 pp. 13570-13575
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Hepatic Lipase Deficiency Increases Plasma Cholesterol but Reduces Susceptibility to Atherosclerosis in Apolipoprotein E-deficient Mice

(Received for publication, January 30, 1997, and in revised form, March 21, 1997)

Hafid Mezdour Dagger , Robert Jones Dagger , Catherine Dengremont , Graciela Castro and Nobuyo Maeda Dagger

From the Dagger  Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, North Carolina 27599-7525 and the  Département d'Athérosclérose U-325, Institut Pasteur, 59019 Lille, France

The effect of hepatic lipase (HL) deficiency on the susceptibility to atherosclerosis was tested using mice with combined deficiencies in HL and apoE. Mice lacking both HL and apoE (hhee) have a plasma total cholesterol of 917 ± 252 mg/dl (n = 24), which is 184% that of mice lacking only apoE (HHee; 497 ± 161 mg/dl, n = 20, p < 0.001). The increase in cholesterol was mainly in beta -migrating very low density lipoproteins, although high density lipoprotein cholesterol (HDLc) was also increased (53 ± 37 versus 20 ± 13 mg/dl, p < 0.01). Despite the increase in plasma cholesterol, we found that HL deficiency significantly decreased aortic plaque sizes in female mice fed normal chow (31 × 103 ± 22 × 103 µm2 in hhee versus 115 × 103 ± 69 × 103 µm2 in HHee, p < 0.001). Reduction of plaque sizes was also observed in female heterozygous apoE-deficient mice fed an atherogenic diet (2 × 103 ± 2.5 × 103 µm2 in hhEe versus 56 × 103 ± 49 × 103 µm2 in HHEe, p < 0.01). Changes in aortic lesion size were not apparent in the small number of male mice studied. In HHee females, both HDLc and the capacity of high density lipoprotein (HDL) particles to promote cholesterol efflux from cultured cells were 26% of the wild type. The absence of HL in hhee females partially restored HDLc levels to 57% and cholesterol efflux to 55% of the wild type. Circulating pre-beta 1-migrating HDL were present in all mutants, suggesting that there are alternative pathways in the formation of these pre-beta -HDL not involving apoE, HL, or cholesteryl ester transfer protein. The improved capacity to promote cholesterol efflux, together with increased HDL, may explain why these animals can overcome the increase in atherogenic lipoproteins.


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