Reversible hyperlipoproteinemia may be observed after ethanol loads in healthy man before any ethanol-induced disease is being established. Different pathogenetic ways to this acute ethanol-induced hyperlipoproteinemia have been investigated or postulated in recent years. Two main sites have appeared: changes in the metabolism of lipids and their precursors which depend from acutal oxidation of ethanol in the liver, and ethanol-induced activation of lipolysis in adipose tissue, transmitted by the sympathico-adrenal system. The changes in liver metabolism during ethanol oxidation have been well confirmed in many experiments, they nevertheless do not seem to lead to hyperlipoproteinemia in many experimental designs in animals and after drinkable amounts of ethanol in healthy man when lipolysis of adipose tissue is blocked and no food is ingested. After the intake of a fatty meal these triglycerides are becoming importance as a source of fatty acids. A possible increased de novo synthesis of palmitic acid may to a minor degree contribute to hypertriglyceridemia.