Abstract:Aim [WT5”BZ]The present study was to compare the clinical efficacy of low dose gemfibrozil with normal dose gemfibrozil administered in hyperlipidemic patients. [WT5”HZ]Methods [WT5”BZ]121 subjects were randomized into two groups: 62 Subjects in low dose gemfribrozil group,59 subjects in normal dose gemfibrozil group as controls. Blood lipid levels were determined prior to lipid lowering treatment and at the end of 4th and 8th week treatment respectively. [WT5”HZ]Results [WT5”BZ] At the end of the 4th week treatment, levels of TC and TG in normal dose gemfibrozil group significantly reduced (P<0.01), and levels of HDLC in normal dose group obviously increased (P<0.01), only levels of TG in low dose group reduced (P<0.05), after treatment compared with the prior to treatmant. At the end of the 8th week treatment, levels of TC and TG significantly reduced and levels of HDLC obviousely increased in both groups. Both of difference were statistically significant (P<0.01). [WT5”HZ]Conclusion [WT5”BZ] Not only was the efficacy of low dose group significantly weaker than that of normal dose group but also the side effects of low dose group was lower

Abstract:Aim To study the mechanism of cholesterol efflux from rat peritoneal macrophages mediated by high density lipoprotein-3(HDL 3). Methods Modification of HDL 3 by N-acetylimidazole blocked interaction between HDL and its cellular receptor. FITC labeled HDL 3 were used to observed the cellular metabolic process of HDL 3. Results BSA (control group) mediated 2.9% cellular cholesterol efflux from the cells. In HDL 3 group and N-acetylimidazole-HDL 3 group,they were 40.7% and 8.7% respectively. After incubation of macrophages with FITC-HDL 3 at 37℃for 3 h, the cell-endocytic fluorescence strength (FS) was 65.0% of the cell-associated FS. When the cells were further incubated with blank media at 37℃for 2 h, 78.4% of the cell-endocytic FS was released into the media. Both the cell-endocytic FS and the cell-released FS were mainly in trichloroacetic acid precepitable form. Conclusions The cellular cholesterol efflux from macrophages mediated by HDL 3 was HDL receptor-dependent. The possible mechanism could be that macrophages internalized HDL 3 by HDL receptor. HDL 3 picked up cellular cholesterol and was resecreted out of cells by a retroendocytic pathway without taking a celluar lysosomal phathway.

Abstract:Aim To determine the allele frequencies of genetic variants 373 Ala→Pro and 451 Arg→Gln of cholesteryl ester transfer protein (CETP) and to explore their potential impacts on serum lipid metabolism. Methods The genotypes in CETP codon 373 and 451 in 91 German healthy students and 409 angiographically confirmed coronary heart disease (CHD) patients were respectively analyzed using the allele specific technique of mutagenically separated polymerase chain reaction (MS-PCR) and their serum lipid parameters were determined.Results It is demonstrated that genetic variants 373 Ala→Pro and 451 Arg→Gln are frequent mutations with allele frequencies around 3% to 5% presented in the healthy individuals as well as in the CHD patients. The high density lipoprotein cholesterol (HDLC) level was significantly decreased in the 373-Pro and 451-Gln alleles heterozygotic carriers in both examined cohorts compared with those in the wild type individuals. The increasing of serum triglyceride (TG) in the mutant alleles carriers was only observed in the healthy volunteers. It was also found that these two genetic variants do not always emerge in the linkage form. Conclusion It is suggested that these two mutations together would possess the phenotype of decreasing HDLC and increasing TG levels.