Effect of Chronic Ethanol Feeding on High Density Lipoprotein Subfractions in Rats

Abstract

We have reported previously that chronic alcohol consumption in the rat produced elevated total serum high density lipoprotein (HDL) fraction, but HDL particles of the alcohol‐fed rat were deficient in apolipoprotein (apo) E. In that report, serum HDL particles were prepared by successive ultracentrifugation method and there were concerns that the apo E deficiency in HDL particles was artificially produced by centrifugal forces. In the present report, apo Al affinity column chromatography was used instead of successive ultracentrifugation and it likewise yielded HDL particles from alcohol‐fed rats that exhibited lower apo E: apo Al ratio than HDL from control rats (0.185 ± 0.016 vs. 0.303 ± 0.017, respectively). When the total serum lipoprotein fraction (d < 1.21) was analyzed by high performance liquid chromatography (HPLC), both HDL and VLDL peaks were higher in alcohol‐fed rats than controls. The size of apo E deficient HDL particles from alcohol‐fed rats determined by HPLC did not differ from that of normal HDL particles. When HDL (1.063 < d < 1.21) was subfractionated into HDL 2 (1.063 < d < 1.125) and HDL 3 (1.125 < d < 1.21), only HDL 2 of alcohol‐fed rats showed lowered apo E: apo Al ratio when compared with same HDL subfraction of control animals. Therefore, the molecular structure of only HDL 2 (but not HDL 3 ) was affected by alcohol‐feeding. Another HDL subpopulation which is enriched with apo E, i.e. HDL 1 (1.054 < d < 1.063), was also prepared. HDL 1 of alcohol‐fed rats was increased by 50% over the controls but its apo E: apo Al ratio was unchanged when compared with control rats. In conclusion, chronic alcohol consumption in the rat produces increased total HDL fraction, decreased apo E: apo Al ratio in the HDL 2 subfraction (1.063 < d 1.125), and increased HDL 1 (1.054 < d < 1.063) subpopulation.