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The effects of the oxidized phospholipids (oxPLs) on amyloid fibril formation by the apolipoprotein A-I variant 1-83/G26R have been investigated using Thioflavin T fluorescence assay. All types of the PoxnoPC assemblies (dispersions, micelles and lipid bilayer vesicles) induced retardation of amyloid nucleation and elongation and the enhancement of the 1-83/G26R fibrillization, although PazePC micelles completely prevented protein aggregation at low protein-to-lipid molar ratios. The ability of PazePC to inhibit 1-83/G26R aggregation was explained by the protein-lipid electrostatic interactions, which either stabilize the a-helical structure of the membrane-associated 1-83/G26R or facilitate the protein solubilization by the detergent micelles. (C) 2017 Elsevier B.V. All rights reserved.

We tested whether hypertriglyceridemia associated with type 2 diabetes mellitus is accompanied by alterations in pre beta-HDL, which are considered to be initial acceptors of cell-derived cholesterol, and by changes in the ability of plasma to promote cellular cholesterol efflux. In 28 hypertriglyceridemic and 56 normotriglyceridemic type 2 diabetic patients, and in 56 control subjects, we determined plasma lipids, HDL cholesterol and phospholipids, plasma pre beta-HDL and pre beta-HDL formation, phospholipid transfer protein (PLTP) activity, plasma cholesterol esterification (EST) and cholesteryl ester transfer (CET) and the ability of plasma to stimulate cholesterol efflux out of cultured human fibroblasts. HDL cholesterol and HDL phospholipids were lower, whereas plasma PLTP activity, EST and CET were higher in hypertriglyceridemic diabetic patients than in the other groups. Pre beta-HDL levels and pre beta-HDL formation were unaltered, although the relative amount of pre beta-HDL (expressed as % of total plasma apo A-I) was increased in hypertriglyeridemic diabetic patients. Cellular cholesterol efflux to plasma from hypertriglyceridemic diabetic patients was increased compared to efflux to normotriglyceridemic diabetic and control plasma, but efflux to normotriglyceridemic diabetic and control plasma did not differ. Multiple linear regression analysis demonstrated that cellular cholesterol efflux to plasma was positively and independently related to pre beta-HDL formation, PLTP activity and EST (multiple r=0.48), but not to the diabetic state. In conclusion, cholesterol efflux from fibroblasts to normotriglyceridemic diabetic plasma is unchanged. Efflux to hypertriglyceridemic diabetic plasma is enhanced, in association with increased plasma PLTP activity and cholesterol esterification. Unaltered pre beta-HDL formation in diabetic hypertriglyceridemia, despite low apo A-I, could contribute to maintenance of cholesterol efflux. (c) 2007 Elsevier Ireland Ltd. All rights reserved.

Background and Aim: HDL-cholesterot (HDL-C) is inversely related to the risk of ischemic heart disease. Many genes are reported to affect HDL-C serum levels in both hyperlipidemic and normolipidemic populations, though the data are controversial. We examined the effect of common gene polymorphisms known to interfere with HDL-C metabolism (apolipoprotein E, cholesterol ester transfer protein and apolipoprotein A-IV gene polymorphisms) on HDL-C plasma levels in normolipidemic subjects. Methods and results: The study population consisted of 200 normolipidernic individuals visiting our clinic for a routine check-up. None of the above gene polymorphisms affected HDL-C levels in our population. However, participants carrying the atlete E4 of the apolipoprotein (apo) E gene, the allele B1 of the TaqIB polymorphisms in the cholesterol ester transfer protein (CETP) gene and the allele T of the apoA-IV gene (A to T polymorphism at site 347) (n=28) had statistically significantly tower HDL-C levels compared to those not carrying the above allele combination (0.99+0.33 vs 1.28 0.35 mmol/L, p=0.04). Conclusion: In this study, we describe a subgroup of normolipidemic individuals with low HDL-C levels due to genetic variability, and we discuss the underlying possible mechanisms involved. (c) 2005 Elsevier Ltd. All. rights reserved. Nutrition Metabolism and Cardiovascular Diseases