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Papers In Press, published online ahead of print December 16, 2002
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Cardiology Dept., Royal Victoria Hospital, Montreal, Quebed H3A 1A1
Corresponding Author: allansniderman{at}hotmail.com
This study determined the effects of apoA1, HDL3 or hydroxy--cyclodextrin on apoB100 secretion and bile acid synthesis by HepG2 cells. The principal observations were that: 1) apoB100 secretion into the medium was significantly less after the addition of any of the three agents. 2) Triglyceride mass was not significantly changed from control in the medium but was significantly, although modestly, reduced in the cells. 3) Neither FC nor CE mass in the medium was changed; by contrast, CE mass was reduced within the cells although FC was not. 4) Although the total mass of cholesterol in the medium was unaffected, the proportion associated with apoB100 was reduced, whereas the proportion associated with the non-apoB100 fraction was increased. 5) There was also an unanticipated, but substantial, increase in bile acid synthesis induced by apoA1, HDL3 or hydroxy--cyclodextrin, which was time and concentration dependent, and which was associated with marked increases in cholesterol 7 -hydroxylase activity. There were no significant changes in ACAT activity and only modest increases in HMG CoA reductase activity. These findings support previous clinical observations that an elevated apoB 100 can accompany a low HDL cholesterol in normotriglyceridemic subjects. They also point to physiologically important, although still only partially understood, metabolic relationships amongst hepatic apoB100 secretion, cholesterol efflux and bile acid synthesis.
Revised on December 6, 2002
Accepted on December 9, 2002
The effects on apoB secretion and bile acid synthesis induced by redirecting cholesterol efflux from HepG2 cells by apoA1, HDL or hydroxy-
cyclodextrin
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