POSTPRANDIAL ELEVATION OF APO-B-48-CONTAINING TRIGLYCERIDE-RICH PARTICLES AND RETINYL ESTERS IN NORMOLIPEMIC MALES WHO SMOKE

Smokers have an increased risk for coronary artery disease (CAD), whic h can only partly be explained by fasting lipoprotein changes. Recent studies have indicated that smokers express metabolic abnormalities ch aracteristic of insulin resistance syndrome. A preliminary study repor ted an increased postprandial triglyceride (TG) response in smokers co mpared with nonsmokers. To investigate the effect of smoking on postpr andial lipemia, a fat-rich mixed meal (837 kcal, 63 g of fat) was serv ed to 12 healthy smokers and 12 controls with similar fasting lipoprot ein profiles, body composition, and lifestyles. Blood was drawn before and 3, 4, 6, and 8 hours postprandially, and triglyceride-rich lipopr otein (TRL) fractions (chylomicrons, VLDL1, VLDL2, and IDL) were separ ated with density gradient ultracentrifugation. Pre-and postprandial T G, retinyl esters (RE), apolipoprotein B-48 (apoB-48) and B-100 (apoB- 100) were measured in each fraction. Smokers showed a significantly in creased postprandial TG response in chylomicrons, VLDL1, and VLDL2. Th e areas under the incremental curve (AUIC) of apoB-48 in chylomicrons (2.83+/-0.84 versus 0.56+/-0.17; P<.05) and VLDL1 (10.17+/-1.96 versus 2.95+/-2.44; P= <.01) were markedly higher in smokers than in control s. Changes of RE responses of all TRL fractions were consistent with t hose of apoB-48. Postprandial apoB-100 concentrations and lipolytic en zymes were similar between the two groups. In conclusion, smokers have the syndrome of impaired TG tolerance because of defective clearance of chylomicrons and their remnants. Prolonged residence time of athero genic remnant particles may constitute a significant risk factor for C AD in smokers.