Plasma Lipid and Lipoprotein Response to Fat Feeding in Alcoholic Liver Disease

Abstract

Serum lipids and lipoproteins were analyzed after an overnight fast, and following a fatty meal in 10 patients with cirrhosis, 5 with fatty liver, and 5 normal subjects. Cirrhotic patients were divided into two groups of five on the basis of serum lecithin-cholesterol acyltransferase activity. Fasting triglyceride levels were similar in all four groups. In all but cirrhotic patients with low lecithin-cholesterol acyltransferase activity, most fasting triglyceride was found in very low density lipoproteins; in the latter group, most of it was found in low density lipoproteins.We confirmed that patients with fatty liver have a higher serum triglyceride response to fat feeding than normal subjects, but we did not find higher levels in cirrhotic patients. Cirrhotic patients with "normal" lecithin-cholesterol acyltransferase activity had a normal triglyceride response to dietary fat. In patients with cirrhosis and low lecithin-cholesterol acyltransferase activity, the increase in triglyceride was less than in normal subjects. In this group, most of the extra triglyceride was carried in low density lipoprotein, and not in chylomicrons and very low density lipoprotein, as in the other groups.It has been known for many years that alcohol ingestion causes fasting hyperlipidemia (1, 2), that alcohol enhances the serum lipid and lipoprotein response to fat meal (3), and that chronic alcohol ingestion causes fatty liver (4). We do not understand how these effects are produced. Some alcoholics develop cirrhosis, and cirrhosis of any cause may be associated with changes in serum lipids and in the structure and composition of serum lipoproteins (5).Borowsky and his colleagues (6) studied the serum lipid and lipoprotein response to fat feeding in patients with alcoholic liver disease. With fatty liver, there was a marked elevation of serum triglyceride after 100 gm of fat. In cirrhotics, the increase was smaller but it was still greater than that found in control subjects. The mechanism of the postprandial triglyceride increase in cirrhosis was not clear. There was no increase in pre-P-lipoprotein, and the changes found in the chylomicron fraction seemed inadequate to account for the rise in serum triglyceride.