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J Biol Chem, Vol. 274, Issue 17, 11564-11572, April 23, 1999
From Two lines of transgenic mice, hAIItg-
Overexpression of Human Apolipoprotein A-II in Mice Induces
Hypertriglyceridemia Due to Defective Very Low Density Lipoprotein
Hydrolysis
,,,,,,,
,,,, and
Unité 505 INSERM, Unité 321 INSERM,
and
hAIItg-
, expressing human apolipoprotein (apo)A-II at 2 and 4 times
the normal concentration, respectively, displayed on standard chow
postprandial chylomicronemia, large quantities of very low density
lipoprotein (VLDL) and low density lipoprotein (LDL) but greatly
reduced high density lipoprotein (HDL). Hypertriglyceridemia may result
from increased VLDL production, decreased VLDL catabolism, or both. Post-Triton VLDL production was comparable in transgenic and control mice. Postheparin lipoprotein lipase (LPL) and hepatic lipase activities decreased at most by 30% in transgenic mice, whereas adipose tissue and muscle LPL activities were unaffected, indicating normal LPL synthesis. However, VLDL-triglyceride hydrolysis by exogenous LPL was considerably slower in transgenic compared with control mice, with the apparent Vmax of the
reaction decreasing proportionately to human apoA-II expression. Human
apoA-II was present in appreciable amounts in the VLDL of transgenic
mice, which also carried apoC-II. The addition of purified apoA-II in postheparin plasma from control mice induced a
dose-dependent decrease in LPL and hepatic lipase
activities. In conclusion, overexpression of human apoA-II in
transgenic mice induced the proatherogenic lipoprotein profile of low
plasma HDL and postprandial hypertriglyceridemia because of decreased
VLDL catabolism by LPL.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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