title: Postprandial cholesteryl ester transfer and high density lipoprotein composition in normotriglyceridemic non-insulin-dependent diabetic patients.
abstract: Altered postprandial HDL metabolism is a possible cause of defective reverse cholesterol transport and increased cardiovascular risk in diabetic patients with a normal fasting lipoprotein profile. Ten normolipidemic, normoponderal non-insulin dependent diabetes mellitus (NIDDM) patients and seven controls received a 980 kcal meal containing 78 g lipids with 100 000 IU vitamin A. Chylomicron clearance was not different, but area under the curve (AUC) for retinyl palmitate in chylimicron-free serum (remnant clearance) was greater in patients (P < 0.02). LCAT activity increased postprandially to the same extent in both groups. In control subjects, cholesteryl ester transfer protein (CETP) activity (CETA) also increased by 20% (P < 0.01 at 6 h) in parallel with a 20% decrease in HDL2-CE (r = -0.55, P = 0.009). In NIDDM patients, on the contrary, CETA which was 35% higher in the fasting state (P < 0.005), decreased postprandially yet HDL2-CE remained unchanged. Postprandial HDL3 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-HDL3 (25.8 +/- 1.7% at 6 h, P < 0.01). These results show that variation in plasma CETA has little impact on HDL2-CE in NIDDH subjects. They support the concept that, in controls, the combined enrichment of HDL3 with PL, increased LCAT and CETA create the conditions for stimulation of cell cholesterol efflux and CE transfer to apo B lipoproteins. In NIDDM, because of the lesser HDL3 enrichment with PL and of the inverse trend of CETA, these conditions fail to occur, depriving the patients of a potentially efficient mechanism of unesterified cholesterol (UC) clearance, despite their strictly normal preprandial profile.
authors.affiliation: Clinique Medicale U 62, Centre Hospitalo-Universitaire de Reims, France.
authors.forename: V
authors.initials: V
authors.lastname: Durlach
authors.forename: N
authors.initials: N
authors.lastname: Attia
authors.forename: A
authors.initials: A
authors.lastname: Zahouani
authors.forename: M
authors.initials: M
authors.lastname: Leutenegger
authors.forename: A
authors.initials: A
authors.lastname: Girard-Globa
mesh_terms: D000328:Adult; D001692:Biological Transport; D001786:Blood Glucose / Q000032:analysis; D002318:Cardiovascular Diseases / Q000453:epidemiology; D002352:Carrier Proteins / Q000097:blood; D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters / Q000097:blood / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D004041:Dietary Fats / Q000493:pharmacokinetics*; D004435:Eating / Q000502:physiology*; D005215:Fasting; D006442:Glycated Hemoglobin / Q000032:analysis; D006023:Glycoproteins; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood*; D008875:Middle Aged; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000097:blood; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood*
chemical_list: D001786:Blood Glucose; D002352:Carrier Proteins; D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters; D004041:Dietary Fats; D006442:Glycated Hemoglobin; D006023:Glycoproteins; D008075:Lipoproteins, HDL; D007862:Phosphatidylcholine-Sterol O-Acyltransferase; D014280:Triglycerides; C506642:CETP protein, human