BACKGROUND: Apolipoprotein (Apo) B-48 is an intestinally derived lipoprotein that is expected to be a marker for cardiovascular disease (CVD). Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a vascular-specific inflammatory marker and important risk predictor of CVD. The aim of this study was to explore the effect of pitavastatin treatment and life style modification (LSM) on ApoB-48 and Lp-PLA2 levels in metabolic syndrome (MS) patients at relatively low risk for CVD, as a sub-analysis of a previous multi-center prospective study. METHODS: We enrolled 75 patients with MS from the PROPIT study and randomized them into two treatment groups: 2 mg pitavastatin daily+intensive LSM or intensive LSM only. We measured the change of lipid profiles, ApoB-48 and Lp-PLA2 for 48 weeks. RESULTS: Total cholesterol, low density lipoprotein cholesterol, non-high density lipoprotein cholesterol, and ApoB-100/A1 ratio were significantly improved in the pitavastatin+LSM group compared to the LSM only group (P≤0.001). Pitavastatin+LSM did not change the level of ApoB-48 in subjects overall, but the level of ApoB-48 was significantly lower in the higher mean baseline value group of ApoB-48. The change in Lp-PLA2 was not significant after intervention in either group after treatment with pitavastatin for 1 year. CONCLUSION: Pitavastatin treatment and LSM significantly improved lipid profiles, ApoB-100/A1 ratio, and reduced ApoB-48 levels in the higher mean baseline value group of ApoB-48, but did not significantly alter the Lp-PLA2 levels.
1-Alkyl-2-acetylglycerophosphocholine Esterase* ; Apolipoprotein B-48* ; Apolipoproteins ; Cardiovascular Diseases ; Cholesterol ; Cholesterol, LDL ; Humans ; Life Style ; Lipoproteins ; Prospective Studies*

BACKGROUND: Omega-3 fatty acids derived from fish oil have been reported to exert a beneficial effect on reducing cardiovascular disease. Reports about their mechanism have generated several interesting findings, including a change in small dense low density lipoprotein (sdLDL) cholesterol proportion, adiponectin, and apolipoprotein B (apoB), in addition to changes in the lipid profile. The principal objective of our study was to evaluate the effects of omega-3 fatty acids on plasma sdLDL, adiponectin, apoB100, and B48 in type 2 diabetic patients with hypertriglyceridemia. METHODS: We randomized 28 type 2 diabetic patients in a placebo-controlled, double-blind trial to receive either omega-3 fatty acids or placebo, both administered at a dose of 4 g daily for 12 weeks. LDL subfractions prior to and after treatment were separated via low-speed ultracentrifugation and analyzed via immunoelectrophoresis. Adiponectin, apoB100, and B48 levels were measured using an ELISA kit. RESULTS: sdLDL proportions were reduced in the omega-3 fatty acids group by 11% after 12 weeks of treatment (n = 17, P = 0.001), and were reduced by 4% in the control group (n = 11, P = 0.096). The patients receiving the omega-3 fatty acids evidenced a significant reduction in the levels of triglyceride (P = 0.001), apoB100, and B48 after 12 weeks (P = 0.038 and P = 0.009, respectively) relative to the baseline. Omega-3 fatty acids supplementation increased fasting blood glucose (P = 0.011), but the levels of HbA1c in each group did not change to a statistically significance degree. The adiponectin value was not reduced in the omega-3 fatty acids group (P = 0.133); by way of contrast, the placebo group evidenced a significant reduction in adiponectin value after 12 weeks (P = 0.002). CONCLUSION: Omega-3 fatty acid treatment proved effective in the reduction of atherogenic sdLDL and apoB in type 2 diabetic patients (Clinical trials reg. no. NCT 00758927, clinicaltrials.gov).
Adiponectin ; Apolipoprotein B-48 ; Apolipoproteins ; Apolipoproteins B ; Blood Glucose ; Cardiovascular Diseases ; Cholesterol ; Diabetes Mellitus, Type 2 ; Enzyme-Linked Immunosorbent Assay ; Fasting ; Fatty Acids, Omega-3 ; Humans ; Immunoelectrophoresis ; Lipoproteins ; Plasma ; Ultracentrifugation

BACKGROUND: The structure of lipoprotein(a) [Lp(a)] includes a low-density lipoprotein cholesterol (LDL-C) component and apolipoprotein(a) [apo(a)] linked to apolipoprotein B-100 of LDL-C with a disulfide bond. Liver cirrhosis is the only disease in which the decrease of serum Lp(a) concentra-tion is observed as a secondary effect. In this study, we tried to investigate the mechanisms for the Lp(a) decrease in cirrhotic patients. METHODS: Forty Child 's class A cirrhotic patients, 40 Child 's class C patients from Asan Medical Center, and 80 healthy controls were recruited. Serum concentrations of interleukin-6 (IL-6), LDL-C, Lp(a), and free apo(a) were measured. RESULTS: The serum concentrations of Lp(a) in the Child 's class C patients were significantly lower than those in class A and the control group (P < 0.05). The apo(a) concentrations in the Child 's class C patients were significantly lower than those in class A and the control group (P < 0.05). The LDL-C concentrations of Child 's class C patients were significantly lower than those in class A and the con-trol group (P < 0.01). The IL-6 concentrations of Child 's class C patients were significantly higher than those in class A and the control group (P < 0.005). Serum concentrations of Lp(a) showed positive correlations with those of LDL-C (r=0.42, P < 0.0001) and with those of the free apo(a) (r=0.68, P < 0.0001). But serum concentrations of IL-6 had no correlation to those of the Lp(a) or the free apo(a). CONCLUSIONS: Considering the positive correlation between Lp(a) and LDL-C, the decrease in the serum Lp(a) in cirrhotic patients could be due mainly to the decrease in the LDL component, although we could not suggest the mechanism for the LDL decrease.
Apolipoprotein B-100 ; Apolipoproteins* ; Apoprotein(a)* ; Child ; Cholesterol ; Cholesterol, LDL* ; Chungcheongnam-do ; Humans ; Interleukin-6 ; Lipoprotein(a)* ; Lipoproteins* ; Liver Cirrhosis* ; Liver*

BACKGROUND AND OBJECTIVES: Little is known about the relationship between the apolipoprotein (apo) B-100, or the apo B-100/apo A-I ratio, and coronary artery disease (CAD). The aim of this study was to investigate this association. SUBJECTS AND METHODS: Our study was carried out on 194 patients who had undergone elective coronary angiography (CAG), but had received no lipid-lowering medication. Patients with acute myocardial infarction were excluded. Stenosis of >or=50% in 1 or more coronary arteries was classified as CAD (+). RESULTS: HDL-C and apo A-I were significantly higher in females than in males (p=0.009 and 0.036). In our population we found that the apo A-I, HDL-C and the apo B-100/apo A-I ratio were significantly related to CAD (p=0.001, 0.006, and 0.007 respectively). In the male group (n=111), the apo B-100/apo A-I ratio was the only parameter statistically significant to CAD after correcting for age, diabetes mellitus and hypertension. Whereas, in the female group (n=83), the apo B/apo A-I ratio, apo B-100/apo A-I ratio, apo B-100, nonHDL-C, triglyceride, apo B, total cholesterol and low-density lipoprotein cholesterol were all significantly related to CAD (p=0.002, 0.003, 0.003, 0.007, 0.007, 0.009, 0.012 and 0.012 respectively). Of these parameters only the apo B-100/apo A-I ratio was significantly related to CAD in both female and male group. CONCLUSION: The apo B-100/apo A-I ratio is an useful indicator for discriminating between CAD (+) and CAD (-).
Apolipoprotein A-I ; Apolipoprotein B-100 ; Apolipoproteins B ; Apolipoproteins* ; Cholesterol ; Constriction, Pathologic ; Coronary Angiography ; Coronary Artery Disease* ; Coronary Disease ; Coronary Vessels* ; Diabetes Mellitus ; Female ; Humans ; Hypertension ; Lipoproteins ; Male ; Myocardial Infarction ; Triglycerides

The work was aimed to investigate the differential expressions of lipid metabolism related genes in the early stage of atherosclerosis in the young apolipoprotein E deficient (apoE(-/-)) mice at different ages with normal chow diet. The genotypes of mice were identified by using multiplex polymerase chain reaction (multi-PCR) analysis. The semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and real-time quantitative RT-PCR were used to analyze the expressions of lipid metabolism related genes in the liver of apoE(-/-) and age-matched wild type (WT) mice of 14-day old, 1-month old, 2-month old, 3-month old. The serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) contents were assayed using COD-PAP and GPO-PAP methods. The serum apolipoprotein B100 (apoB100) content was quantitated by immune turbidimetry. The hearts were perfusion-fixed in 4% formaldehyde, infiltrated with 30% gum sucrose for 24 h at 4 °C, and embedded in OCT compound. The aortic sinus tissues were serially sectioned at -15 °C, stained with Sudan IV, and counterstained with light green. The results were shown as follows. Compared with that in WT mice, the mRNA levels of apoA I and apoA IV in apoE(-/-) mice aged from 14-day old to 3-month old changed prominently (P<0.05), with apoA I up-regulated and apoA IV down-regulated. At the age of 1 month, the expression of apoB100 in apoE(-/-) mice was higher than that in WT mice (P<0.05). The expression of apoA V was up-regulated (P<0.05) and there was obvious lipid deposition in the aortic intima in apoE(-/-) mice at the age of 2 months. The expressions of fatty acid translocase (Fat/CD36) and angiopoietin-like protein 3 (Angptl 3) in apoE(-/-) mice were higher than those in WT mice at the age of 3 months (P<0.05), while the expressions of peroxisome proliferator-activated receptor α (PPARα), liver X receptor α (LXRα), carnitine palmitoyl transferase I (CPT I) and acyl coenzyme A oxidase 1 (ACOX1) showed no significant changes. The serum TC, TG, LDL-C and HDL-C contents in apoE(-/-) mice aged from 14-day old to 3-month old were higher than those in age-matched WT mice. apoE(-/-) mice showed a marked increase in serum apoB100 content, consistent with the trend of serum LDL-C content and apoB100 mRNA content in the liver. The results suggest that the mRNA expressions of apoA I, apoA IV, apoA V, apoB100 and Angptl 3 in apoE(-/-) mice change significantly compared with those in WT mice, and these genes might be relevant to the complicated lipid metabolism network, and involved in the early stage of atherogenesis.
Animals ; Apolipoprotein A-I ; metabolism ; Apolipoprotein B-100 ; blood ; Apolipoproteins A ; metabolism ; Apolipoproteins E ; genetics ; Atherosclerosis ; genetics ; Gene Expression ; Lipid Metabolism ; genetics ; Lipoproteins, HDL ; blood ; Lipoproteins, LDL ; blood ; Liver ; metabolism ; Mice ; Mice, Knockout ; Triglycerides ; blood

<b>OBJECTIVEb>To explore the relationship between the expression characteristics of lipid metabolism-related genes in the liver and early atherosclerotic lesions in apolipoprotein E and low density lipoprotein receptor gene double knockout (apoE(-/-)/LDLR(-/-)) mice.

<b>METHODSb>RT-PCR was used to detect the differential expression of lipid metabolism-related genes in the liver of apoE(-/-)/LDLR(-/-) and wild type (WT) mice. Serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) level as well as aortic morphology were also analyzed.

<b>RESULTSb>Among the 11 lipid metabolism-related genes, apolipoprotein B100 (apoB100) mRNA levels were significantly higher in apoE(-/-)/LDLR(-/-)mice compared with WT mice. At 14 days, 1, 2 and 3 months of age, the level of mRNA expression were 1.55, 1.47, 1.50 and 2.42 folds of those of the age matched WT mice respectively. The fatty acid transporter (FAT/CD36) mRNA expression levels were higher in 14-day and 3-month old mice at 1.30 and 1.35 folds of those of the age matched WT mice, respectively. Apolipoprotein A IV (apoA IV) and Apolipoprotein AV (apoAV) mRNA levels were significantly down-regulated (0.89 fold decrease in 14-day, and 0.90 folds decrease in 3-month, respectively). The mRNA expression levels of apolipoprotein AI (apo AI), apolipoprotein F (apo F), peroxidase proliferator-activated receptor alpha (PPAR-alpha), liver X receptor alpha (LXRalpha), angiopoietin-like protein 3 (ANGPTL3), acyl-coenzymeA oxidase 1 (ACOX1) and carnitine palmitoyl transferase 1 (CPT1) had no significant changes. Serum TC, TG and LDL-C were higher than those of age matched WT mice at 7, 2 and 30 folds, respectively. Furthermore, apoE(-/-)/LDLR(-/-) mice demonstrated typical early atherosclerotic lesions at sinus and root regions of aorta in an age dependent manner.

<b>CONCLUSIONb>Alterations of the expression of lipid metabolism-related genes in liver play important roles in the development of AS in the apoE(-/-)/LDLR(-/-) mice at early ages.

Animals ; Aorta ; pathology ; Apolipoprotein A-V ; Apolipoprotein B-100 ; biosynthesis ; genetics ; Apolipoproteins ; biosynthesis ; genetics ; Apolipoproteins A ; biosynthesis ; genetics ; Apolipoproteins E ; deficiency ; Atherosclerosis ; etiology ; metabolism ; pathology ; CD36 Antigens ; biosynthesis ; genetics ; Gene Expression ; Lipid Metabolism ; Liver ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; RNA, Messenger ; metabolism ; Receptors, LDL ; deficiency

Serum levels of apolipo protein A-I (Apo A-I) and apolipo protein B (Apo B) were determined with immumo turbidimetry technique on 42 healthy subjects. Obtained Apo AI values were distributed according to standard Gauss rule. Apo AI values were determined in the interval of 87-94 mg/dl, and Apo B- 57.112 mg/dl. There was no difference between male and female subjects in terms of serum levels of Apo B and Apo A-I. The results could be approved temporarily as reference for laboratory and clinical works
Serum ; Apolipoprotein A-I ; Apolipoproteins B

<b>OBJECTIVEb>To investigate the relationship between G1025C (Try316Ser) polymorphism in exon 8 of apolipoprotein H (apoH) gene and stroke and to evaluate the effect of G1025C(Try316Ser) polymorphism on plasma lipid levels in Changsha Hans.

<b>METHODSb>G1025C (Try316Ser) polymorphism in apoH gene was determined by PCR-single strand conformation polymorphism analysis and DNA sequencing in 100 healthy controls, 260 patients with stroke, and 20 stroke pedigrees. Serum antiphospholipid antibody (APA) levels were tested by enzyme linked immunosorbent assay (ELISA). Plasma lipid levels were measured by routine methods.

<b>RESULTSb>No statistically significant differences were found in frequencies of genotypes and alleles of G1025C (Try316Ser) polymorphism between the controls and stroke patients. The serum levels of TG in the GC genotype of cerebral infarction patients and controls were markedly higher than those in GG genotype.

<b>CONCLUSIONb>There was no association betweenG1025C (Try316Ser) polymorphism and stroke in Changsha Hans. G1025C (Try316Ser) polymorphism was associated with plasma lipid metabolism in Changsha Hans.

Adult ; Aged ; Alleles ; Apolipoprotein A-I ; blood ; Apolipoprotein B-100 ; Apolipoproteins B ; blood ; Base Sequence ; Cerebral Hemorrhage ; complications ; Cerebral Infarction ; complications ; China ; Cholesterol ; blood ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; DNA ; chemistry ; genetics ; DNA Mutational Analysis ; Female ; Gene Frequency ; Genotype ; Glycoproteins ; genetics ; Humans ; Lipids ; blood ; Lipoprotein(a) ; blood ; Male ; Middle Aged ; Mutation, Missense ; Polymorphism, Genetic ; Polymorphism, Single-Stranded Conformational ; Stroke ; blood ; etiology ; genetics ; Triglycerides ; blood ; beta 2-Glycoprotein I

The hepatitis C virus (HCV) is a globally prevalent human pathogen that causes persistent liver infections in most infected individuals. Several studies reported that HCV particles are enriched in apolipoprotein E (apoE) and that apoE is required for HCV infectivity and production. However, the relationship between apoE gene polymorphisms and HCV genotypes in patients with HCV is less well understood. The aim of this study was to investigate the association between apoE gene polymorphism and HCV genotypes in patients. The HCV genotypes were identified among the 124 patients infected with HCV, and the genetic characteristics of the HCV genotype were analyzed. In addition, the results of the clinical laboratory test were comparatively analyzed according to the classified genotypes. Both HCV 1b (n=80) and 2a (n=42) patients had higher AFP, AST, ALT, ALP, γ-GTP, apoB, and apoE values compared with the normal control group. In particular, apoB and apoE levels were statistically significantly higher in the HCV 2a patients (P<0.05) and apoE levels were significantly higher in the HCV 1b patients (P<0.000). According to the results the patients with HCV genotype 1b showed higher values of liver damage related indicators and apoB expression than the patients with HCV genotype 2a. The fat related indicators and apoE expression were not different between the two major HCV genotypes (2a and 1b). We anticipate that the apoE ε3 allele is the most common type in HCV genotype 1b (89.2%) and 2a (91.7%). As a result of apoE genotyping, we confirmed an association with HCV infection and the apoE ε3 allele. However, the ratios of the apoE ε3 allele among the patients with genotype 1b and 2a were similar to each other.
Alleles ; Apolipoproteins B ; Apolipoproteins E ; Apolipoproteins ; Genotype ; Hepacivirus ; Hepatitis C ; Hepatitis ; Humans ; Liver

Apolipoproteins B ; metabolism ; Atherosclerosis ; metabolism ; Humans