Differences in postprandial concentrations of very-low-density lipoproteinand chylomicron remnants between normotriglyceridemic and hypertriglyceridemic men with and without coronary heart disease

It has been suggested that the postprandial elevation of plasma triglycerid es is more closely linked to coronary heart disease (CHD) than the fasting triglyceride level. However, the postprandial situation is complex, as hepa togenous triglyceride-rich lipoprotein (TRL) particles (apolipoprotein [apo ]B-100 and very-low-density lipoprotein [VLDL]) are mixed in the blood with apoB-48-containing lipoproteins secreted from the intestine. To analyze th e relative proportion of liver-derived and intestinal apoB-containing TRL i n subjects with and without CHD, we performed standardized oral fat-loading tests in young survivors of myocardial infarction, a large proportion of w hom are hypertriglyceridemic (HTG), as well as sex- and population-matched healthy control subjects. A special effort was made to recruit healthy HTG subjects as controls for the HTG patients. Easting plasma triglycerides (3. 74 +/- 1.35 v 3.01 +/- 0.83, NS), low-density lipoprotein (LDL) cholesterol , and VLDL lipids, and apoB-100 and apoB-48 content at Svedberg flotation r ate (Sf) 60-400, Sf 20-60, and Sf 12-20 did not differ between HTG patients (n = 10) and HTG controls (n = 14). Normotriglyceridemic (NTG) patients (n = 15) had higher fasting plasma triglycerides (1.44 +/- 0.39 v 0.98 +/- 0. 33 mmol/L, P < .05) and LDL cholesterol (4.07 +/- 0.71 v 3.43 +/- 0.64, P < .05) than NTG controls (n = 34). The triglyceride elevation was accounted for by a higher level of small VLDL (apoB-100 in the Sf 20-60 fraction, 52 +/- 17 v 29 +/- 20 mg/L, P < .05). HTG patients responded with clearly elev ated plasma triglycerides in the late postprandial phase, ie, 7, 8, and 9 h ours after fat intake. Essentially, this was explained by a retention of la rge VLDL particles, since HTG patients exhibited no major differences in ap oB-48 concentrations in the Sf > 400, Sf 60-400, and Sf 20-60 fractions but showed marked differences in the level of apoB-100 at Sf 60-400 (large VLD L) 9 hours after fat intake when compared with HTG controls (101 +/- 13 v 5 7 +/- 5 mg/L, P < .01). NTG patients were characterized by a more rapid inc rease of large VLDL in the early postprandial state, ie, 3 hours after fat intake, with a mean increase from baseline to 3 hours of 24.1 +/- 6.7 mg/L for NTG patients and 11.8 +/- 2.0 mg/L for controls (P < .05). ApoB-48 leve ls were also slightly higher, but all TRL parameters returned to baseline w ithin 9 hours after fat intake. In conclusion, elevated triglyceride levels in the postprandial state in CHD patients are explained to a large extent by the accumulation of endogenous TRL. This suggests that the postprandial dyslipidemia encountered in CHD is more dependent on a failure of regulatio n of endogenous TRL versus the exogenous TRL species. Copyright (C) 1999 by W.B. Saunders Company.