PO2-33 THE INCREASE OF APOA-V DURING POSTPRANDIAL LIPEMIA FOLLOWS THE RESPONSE OF TRIGLYCERIDE-RICH LIPOPROTEINS (TRL) IN TYPE 2 DIABETES

Abstract

The sequence of alterations in the concentration and composition of different plasma lipoproteins following alcohol intake is not known. We therefore monitored the concentrations of cholesterol, triglycerides, phospholipids, and proteins in the major lipoprotein fractions (VLDL, LDL, HDL2, and HDL3) in ten nonalcoholic healthy male volunteers who were given 5.5 g of alcohol per kilogram of body weight during 212days (a weekend). In addition, lipoprotein lipase activity was measured in post-heparin plasma and in adipose tissue and hepatic lipase activity was measured in post-heparin plasma before and after the experiment. In a separate control experiment, the same subjects received meals and liquids without alcohol. Blood alcohol levels remained below 1.5 g/L. Alcohol caused a progressive increase in the fasting VLDL triglyceride and phospholipid concentrations, both of which were doubled during the experiment (P < 0.001). In contrast, the VLDL cholesterol levels remained unchanged until the third morning, when there was a slight increase. The LDL triglyceride and phospholipid concentrations also rose without simultaneous changes in the LDL cholesterol concentration. Consistent with these changes, the HDL cholesterol concentration showed no response to alcohol during the experiment, but the HDL phospholipid level rose from 76 to 99 mg/dL (P < 0.001). This was reflected as an increase in the HDL2 concentration from 124 to 158 mg/dL (P < 0.01), whereas no change occurred in the HDL3 level. The increment of HDL2 concentration was due to a rise of its triglycerides, phospholipids, and apoproteins A-I and A-II but not to a rise of cholesterol. Thus, the VLDL, LDL and HDL2 fractions all became relatively depleted of cholesterol during alcohol intake. Alcohol potentiated the postprandial rise of plasma triglycerides with an increase in triglyceride concentrations in all lipoprotein fractions. During alcohol intake the HDL2 concentration increased postprandially (P < 0.05) whereas the HDL3 concentration decreased slightly, the fall being accounted for by a decrease in the HDL3 cholesterol level. The lipoprotein lipase activity of adipose tissue increased by an average of 2.3-fold (P < 0.01) over the alcohol-intake period, whereas the postheparin plasma hepatic lipase activity fell by 28% (P < 0.01). The results support the hypothesis that alcohol initially stimulates the secretion of VLDL particles that contain less cholesterol than “normal” VLDL. As a consequence of this and of a concomitant induction of lipoprotein lipase, alcohol intake is followed by an accelerated transfer of the VLDL catabolic products to HDL and by a subsequent rise in the levels of HDL2 triglycerides, phospholipids, and apoproteins but not of cholesterol. The suppression of hepatic lipase activity by alcohol may contribute further to the rise of HDL2 phospholipids. It thus appears that the increase of HDL cholesterol is a late phenomenon being expressed only after more prolonged use of alcohol.