P. Marmillot et al., Effect of dietary omega-3 fatty acids and chronic ethanol consumption on reverse cholesterol transport in rats, METABOLISM, 49(4), 2000, pp. 508-512
We previously showed that chronic ethanol feeding reads to a decrease of ap
olipoprotein E (apoE) in high-density lipoprotein (HDL), whereas supplement
ing this diet with 2.8% of total dietary calories as omega 3-fatty acids (o
mega 3FAs) restores HDL-apoE to the control values. Since HDL containing ap
oE plays a major role in reverse cholesterol transport (RCT), we measured t
he effects chronic ethanol intake and omega 3-FAs -FAs on RCT in the presen
t study. Four groups of rats, control normal fat (CN), alcohol-normal fat (
AN), control omega 3FA fat (CF), and alcohol-omega 3FA fat (AF), were fed t
heir respective diets for 8 weeks, after which hepatocytes and HDLs from ea
ch group were evaluated for RCT capacity (cholesterol efflux from macrophag
es end uptake by liver cells). Compared with the control diet (CN), chronic
ethanol (AN) feeding inhibited the cholesterol efflux capacity of HDL by 2
1% (P <.01), whereas w3FA feeding (2.8% of total dietary calories) stimulat
ed this capacity by 79% (P <.01) and 25% (P <.01) in CF and AF rats, respec
tively. With respect to cholesterol uptake by the liver, there were no sign
ificant 3-way or 4-way interactions between the 4 factors, HDL-alcohol, MDL
-fish oil, hepatocyte-alcohol, and hepatocyte-fish oil. The main effects fo
r HDL-alcohol, HDL-fish oil, and hepatocyte-alcohol were all highly signifi
cant (P =.0001,.0001, and .007, respectively). There was a significant HDL-
alcohol and HDL-fish oil interaction (P =.0001). Hepatocyte-alcohol was not
a factor in any 2-way interactions. Our study indicates no evidence of an
interaction between the effects of omega 3FAs end the effects of alcohol on
hepatocytes in terms of RCT function. Thus, feeding as little as 2.8% of t
he total dietary calories as w3FA not only restored the impaired RCT functi
on of HDL caused by chronic ethanol intake, but also enhanced by severalfol
d the ability of HDL to promote RCT even in normal animals. Copyright (C) 2
000 by W.B. Saunders Company.