4.7 Article

Effect of dietary omega-3 fatty acids and chronic ethanol consumption on reverse cholesterol transport in rats

Journal

METABOLISM-CLINICAL AND EXPERIMENTAL
Volume 49, Issue 4, Pages 508-512

Publisher

W B SAUNDERS CO
DOI: 10.1016/S0026-0495(00)80017-7

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We previously showed that chronic ethanol feeding reads to a decrease of apolipoprotein E (apoE) in high-density lipoprotein (HDL), whereas supplementing this diet with 2.8% of total dietary calories as omega 3-fatty acids (omega 3FAs) restores HDL-apoE to the control values. Since HDL containing apoE plays a major role in reverse cholesterol transport (RCT), we measured the effects chronic ethanol intake and omega 3-FAs -FAs on RCT in the present 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 their respective diets for 8 weeks, after which hepatocytes and HDLs from each group were evaluated for RCT capacity (cholesterol efflux from macrophages end uptake by liver cells). Compared with the control diet (CN), chronic ethanol (AN) feeding inhibited the cholesterol efflux capacity of HDL by 21% (P <.01), whereas w3FA feeding (2.8% of total dietary calories) stimulated this capacity by 79% (P <.01) and 25% (P <.01) in CF and AF rats, respectively. With respect to cholesterol uptake by the liver, there were no significant 3-way or 4-way interactions between the 4 factors, HDL-alcohol, MDL-fish oil, hepatocyte-alcohol, and hepatocyte-fish oil. The main effects for HDL-alcohol, HDL-fish oil, and hepatocyte-alcohol were all highly significant (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 the total dietary calories as w3FA not only restored the impaired RCT function of HDL caused by chronic ethanol intake, but also enhanced by severalfold the ability of HDL to promote RCT even in normal animals. Copyright (C) 2000 by W.B. Saunders Company.

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