Relationship of alcoholic hypertriglyceridemia to stage of liver disease and dietary lipid.

To clarify contributions of alcoholic liver injury, dietary fat and acute ethanol intake to alcoholic hypertriglyceridemia, control subjects and alcoholics with fatty liver or cirrhosis were given a high fat meal with and without ethanol. The triglyceridemic response to the meal in patients with fatty liver (551.3 +/- 98.4 mg x hr/dl) was enhanced compared to controls (106.4 +/- 30.9) and characterized by increased fasting and postprandial pre-beta lipoproteins. The cirrhotics' response (262.5 +/- 34.9) was characterized by minimal fasting and postprandial pre-beta lipoproteins and increased postmeal chylomicrons. Ethanol added to the meal enhanced the lipemic response of controls, barely altered the response of patients with fatty liver, and decreased the response of cirrhotics. In an expanded group of alcoholic patients, the percentage of pre-beta lipoproteins determined by electrophoresis reflected the degree of liver injury. Therefore, major determinants of alcoholic triglyceridemia are stage of liver injury and dietary lipid; electrophoretic determination of pre-beta lipoproteins may indicate degree of alcoholic liver damage.