Microsomal induction, alcohol, and lipoprotein metabolism: is there a three-way relationship?

The role of ethanol as a microsomal enzyme-inducing agent and as a modulator of lipid metabolism is reviewed. In an attempt to ascertain the mechanisms underlying the latter effects we examined the changes in hepatic triglyceride lipase (HTGL), hepatic high density lipoprotein (HDL) binding, and apolipoprotein secretion mediated by ethanol in a variety of experimental situations. Chronic administration of ethanol to rats decreased the ability of the liver to secrete HTGL, but primary liver cultures prepared from both ethanol and sucrose-fed rats secreted more HTGL when acutely exposed to ethanol over a 3-day period than when grown in a control medium. Hep G2 cells when grown in ethanol-containing medium for 14-28 days manifested increased HDL-binding capacity; apolipoprotein-A1 secretion was increased by ethanol but apolipoprotein B secretion was not affected. These findings suggest that increased plasma HDL concentrations which follow chronic ethanol ingestion may be due, at least in part, to increased hepatic secretion and reduced intravascular conversion of the lipoprotein despite enhanced reuptake by the liver; they are not consistent with an ethanol-mediated alteration in very low density lipoprotein secretion by the liver.