POSTPRANDIAL CHOLESTERYL ESTER TRANSFER AND HIGH-DENSITY-LIPOPROTEIN COMPOSITION IN NORMOTRIGLYCERIDEMIC NON-INSULIN-DEPENDENT DIABETIC-PATIENTS

Altered postprandial HDL metabolism is a possible cause of defective r everse cholesterol transport and increased cardiovascular risk in diab etic patients with a normal fasting lipoprotein profile. Ten normolipi demic, normoponderal non-insulin dependent diabetes mellitus (NIDDM) p atients and seven controls received a 980 kcal meal containing 78 g li pids with 100 000 IU vitamin A, Chylomicron clearance was not differen t. but area under the curve (AUC) for retinyl palmitate in chylimicron -free serum (remnant clearance) was greater in patients (P < 0.02), LC AT activity increased postprandially to the same extent in both groups . In control subjects, cholesteryl ester transfer protein (CETP) activ ity (CETA) also increased by 20% (P < 0.01 at 6 h) in parallel with a 20% decrease in HDL(2)-CE (r = -0.55, P = 0.009). In NIDDM patients, o n the contrary, CETA which was 35% higher in the fasting slate (P < 0. 005), decreased postprandially yet HDL(2)-CE remained unchanged. Postp randial HDL(3) of controls were enriched with phospholipid (PL) (30.3 +/- 2.6% at 6 h) with respect to fasting (25.6 +/- 2.5%, P < 0.01) and to NIDDM-HDL(3) (25.8 +/- 1.7% at 6 h, P < 0.01). These results show that variation in plasma CETA has little impact on HDL(2)-CE in NIDDH subjects. They support the concept that, in controls, the combined enr ichment of HDL(3) with FL, increased LCAT and CETA create the conditio ns for stimulation of cell cholesterol efflux and CE transfer to apo B lipoproteins. In NIDDM, because of the lesser HDL(3) enrichment with PL and of the inverse trend of CETA, these conditions fail to occur, d epriving the patients of a potentially efficient mechanism of unesteri fied cholesterol (UC) clearance, despite their strictly normal prepran dial profile.