Apolipoproteins B ; metabolism ; Atherosclerosis ; metabolism ; Humans

BACKGROUND: Psoriasis is a disease of unknown etiology. Disturbances in lipid metabolism have been suggested as a possible pathogenetic mechanism. OBJECTIVE: The study was performed to investigate the blood lipid, lipoprotein and apolipo-protein levels and their difference according to family history in Korean psoriasis patients. METHODS: Blood samples from seventy three psoriasis patients and twenty three normal persons were measured for total ciolesterol(TC), VLDL-cholesterol(VLDL-C), LDL-cholesterol(LDL-C), HDL-cholesterol(HDL-C), lipoprotein(a) (LPA), triglyceride(TG), apolipoprotein A-I(APO-AI), and apolipoprotein B(AFO-B). Psoriasis patients were divided according to their family history of psoriasis. RESULTS: Compared to ccntrols, TC, LDL-C, LPA, TG, APO-B were significantly elevated in psoriasis patients. Mean varues of LPA and APO-B in psoriasis group were above normal range. VLDL-C were significasitly elevated only in female patients. There was a tendency for psoriasis patients with family history to have higher values than those without family history. CONCLUSION: TC, LDL-C, L,PA, TG, APO-B was increased in psoriasis, especially in the patients with family history, cornpared to control. It is recommended that we must pay attention to the possible risk for the development of cardiac or cerebral vascular disease in psoriasis patients, especially in the presence of family history of psoriasis.
Apolipoproteins ; Apolipoproteins B ; Female ; Humans ; Lipid Metabolism ; Lipoprotein(a) ; Lipoproteins* ; Psoriasis* ; Reference Values ; Vascular Diseases

PURPOSE: The increased prevalence of dyslipoproteinemia in obese children probably contributes to the high risk of cardiovascular disease associated with being overweight. The genetic makeup is possible one of the factors that influence the impact of obesity on lipid metabolism. A relation between apolipoprotein E (Apo E) polymorphism and lipid metabolism has been convincingly demonstrated in large population. The purpose of this study was to determine whether Apo E polymorphism also influences the risk of dyslipidemia in obese children. METHODS: We studied 89 obese children with weight-for-height excess of 40% by obesity index. We measured the serum concentration of total cholesterol, triglyceride, HDL-cholesterol, LDL- cholesterol, Lipoprotein (a) (Lp(a)), apolipoprotein A (Apo A) and Apo B after overnight fasting. Apo E gene polymorphism of the 89 obese children and 30 control students were analyzed by ARMS (amplication refractory mutation system) method. RESULTS: The frequency of etsilon2, etsilon3, and etsilon4 allele were 9.7%, 82.3% and 8.0%, respectively in children. There was no significant difference between Apo E allele frequency of obese children and those of nonobese children. The serum concentrations of total cholesterol, LDL-cholesterol and Apo B were lower in etsilon2 genotype. The obese children with etsilon4 genotype had higher frequency of hypertriglyceridemia, increased level of Lp(a) and decreased level of HDL-cholesterol than other types. There was no evidence of EKG abnormality and cardiovascular complications in obese children. CONCLUSION: Our data demonstrated that obesity is associated with an increase in the risk of lipoprotein abnormalities and that the serum concentrations of total cholesterol, LDL-cholesterol and Apo B were influenced by Apo E genotypes.
Alleles ; Apolipoproteins B ; Apolipoproteins E ; Apolipoproteins* ; Arm ; Cardiovascular Diseases ; Child* ; Cholesterol ; Dyslipidemias ; Electrocardiography ; Fasting ; Gene Frequency ; Genotype ; Humans ; Hypertriglyceridemia ; Lipid Metabolism ; Lipoprotein(a) ; Lipoproteins ; Obesity ; Overweight ; Plasma* ; Prevalence ; Triglycerides

Accelerated atherosclerosis is not only a frequent complication but also the most common cause of death in patients with chronic renal failure (CRF). Although mechanisms are unclear, disorder of lipid metabolism may be a major factor. Since apolipo-protein (apo) E is known to play a major regulatory role in lipid metabolism, we evaluated apo E genotype in 72 male patients with CRF and compared with that in 194 rnale normal controls. In addition, we measured plasma lipid and apolipoprotein concentrations and evaluated them according to apo E genotype in patients and controls. Apo E genotype was determined with the INNO-LiPA Apo E kit (Innogenetics, Belgium), which is based on reverse hybridization. The results are as follows ; 1) The distribution of the three major apo E alleles in patients with CRF ( e 2: 6.2%, e 3: 80.6%, e 4: 13.2%) was not different from that in controls ( e 2: 4.1%, e 3: 87.6%, e 4: 8.3%). 2) In patients with CRF, total cholesterol, lowdensity lipoprotein (LDL) and high-density lipoprotein (HDL) levels were significantly lower and the triglyceride and lipoprotein (a) levels were significantly higher than those in controls. 3) In controls, E 4/3 group had significantly lower levels of HDL than E 3/3 and E 3/2 groups. In patients with CRF, E 4/3 group had significantly higher levels of total cholesterol and apo B lipoprotein than E3/2 group. In conclusion, although there was no significant difference in the apo E genotype frequencies between male patients with CRF and controls, apo E polymorphism may play an important role in the determination of individual differences in plasma lipids in male patients with CRF.
Alleles ; Apolipoproteins B ; Apolipoproteins E ; Apolipoproteins* ; Atherosclerosis ; Cause of Death ; Cholesterol ; Genotype ; Humans ; Individuality ; Kidney Failure, Chronic* ; Lipid Metabolism ; Lipoprotein(a) ; Lipoproteins ; Male* ; Plasma* ; Triglycerides

BACKGROUND/AIMS: Changes in lipid profiles in patients infected with hepatitis C virus (HCV) during direct-acting antiviral therapy have been reported in recent years. However, the clinical aspects of disturbed lipid metabolism in chronic HCV infection have not been fully elucidated. METHODS: Dynamic changes in serum total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol and apolipoprotein levels in patients infected with HCV genotype 1b were examined during combination therapy with daclatasvir (DCV) and asunaprevir (ASV). RESULTS: Total, LDL−, and HDL-cholesterol levels increased rapidly and persistently after week 4. Apolipoprotein (apo) A-I, apo B, apo C-II, and apo C-III levels were significantly higher at week 4 than at week 0. In contrast, apo A-II and apo E levels were significantly lower. The differences in LDL− and HDL-cholesterol levels were positively correlated with those of apo B and apo A-I, respectively. Interestingly, in patients with non-sustained virological response, these cholesterol levels decreased rapidly after viral breakthrough or viral relapse. Furthermore, similar changes were observed for apo A-I, apo B and apo C-III levels. CONCLUSIONS: Clearance of HCV using combination therapy with DCV and ASV results in rapid changes in serum lipid profiles, suggesting an influence of HCV infection on disturbed lipid metabolism.
Apolipoprotein A-I ; Apolipoprotein A-II ; Apolipoprotein C-II ; Apolipoprotein C-III ; Apolipoproteins ; Apolipoproteins B ; Apolipoproteins E ; Cholesterol ; Genotype ; Hepacivirus* ; Hepatitis C* ; Hepatitis* ; Humans ; Lipid Metabolism ; Lipoproteins ; Recurrence

PURPOSE: Apolipoprotein E (Apo E) plays a major role in lipoprotein metabolism and lipid transport. Many investigators have described that Apo E polymorphisms is one of the most important genetic determinants for cardiovascular disease. The purpose of this study was to evaluate the association between Apo E polymorphisms and serum lipid profiles in obese adolescent. METHODS: We measured the serum concentrations of glucose, apolipoprotein (Apo) A1, Apo B, total cholesterol (TC), triglyceride (TG), HDL and LDL-cholesterol after overnight fasting in obese adolescent. Apo E polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: 86 obese adolescents participated in this study. The body mass index (BMI) of participants were excess of 95 percentile by age and sex. Male to female ratio was 1.7 and mean age of study group was 16.2+/-1.8 years. Mean BMI was 27.4+/-2.5 kg/m2. The frequency of epsilon2, epsilon3 and epsilon4 allele were 8.1%, 87.2% and 4.7% respectively. Study populations were classified into the following three genotypes 1) Apo E2 group (n=13, 15.1%) carrying either the epsilon2/epsilon2 or epsilon2/epsilon3 2) Apo E3 group (n=65, 75.6%) carrying the most frequent epsilon3/epsilon3 3) Apo E4 group (n=8, 9.3%) carrying either the epsilon3/epsilon4 or epsilon4/epsilon4. No differences were found among Apo E genotypes concerning age, sex, weight, height and BMI. Apo B and LDL-cholesterol concentrations were significantly higher in the Apo E4 group (P<0.05). No association were found between Apo E genotypes and glucose, Apo A1, TC, TG and HDL. CONCLUSIONS: We confirmed that serum concentrations Apo B and LDL-cholesterol were influenced by Apo E genotypes. Apo E polymorphisms seems to influence some alteration of lipid metabolism associated with obesity in adolescent.
Adolescent ; Alleles ; Apolipoprotein A-I ; Apolipoprotein E2 ; Apolipoprotein E3 ; Apolipoprotein E4 ; Apolipoproteins ; Apolipoproteins B ; Apolipoproteins E ; Body Mass Index ; Cardiovascular Diseases ; Cholesterol ; Fasting ; Female ; Genotype ; Glucose ; Humans ; Lifting ; Lipid Metabolism ; Lipoproteins ; Male ; Obesity ; Research Personnel

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>We aimed to investigate the cumulative effect of high CRP level and apolipoprotein B-to-apolipoprotein A-1 (ApoB/ApoA-1) ratio on the incidence of ischemic stroke (IS) or coronary heart disease (CHD) in a Mongolian population in China.

<b>METHODSb>From June 2003 to July 2012, 2589 Mongolian participants were followed up for IS and CHD events based on baseline investigation. All the participants were divided into four subgroups according to C-reactive protein (CRP) level and ApoB/ApoA-1 ratio. Cox proportional hazard models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for the IS and CHD events in all the subgroups.

<b>RESULTSb>The HRs (95% CI) for IS and CHD were 1.33 (0.84-2.12), 1.14 (0.69-1.88), and 1.91 (1.17-3.11) in the 'low CRP level with high ApoB/ApoA-1', 'high CRP level with low ApoB/ApoA-1', and 'high CRP level with high ApoB/ApoA-1' subgroups, respectively, in comparison with the 'low CRP level with low ApoB/ApoA-1' subgroup. The risks of IS and CHD events was highest in the 'high CRP level with high ApoB/ApoA-1' subgroup, with statistical significance.

<b>CONCLUSIONb>High CRP level with high ApoB/ApoA-1 ratio was associated with the highest risks of IS and CHD in the Mongolian population. This study suggests that the combination of high CRP and ApoB/ApoA-1 ratio may improve the assessment of future risk of developing IS and CHD in the general population.

Adult ; Apolipoproteins A ; classification ; genetics ; metabolism ; Apolipoproteins B ; genetics ; metabolism ; C-Reactive Protein ; genetics ; metabolism ; Cohort Studies ; Coronary Disease ; epidemiology ; etiology ; Gene Expression Regulation ; Humans ; Mongolia ; epidemiology ; Prospective Studies ; Risk Factors ; Stroke ; epidemiology ; etiology ; Young Adult

<b>OBJECTIVEb>To observe the histopathological features, nuclear factor-κB (NFκB) and IKB expressions as well as calcium deposition of atherosclerosis plaques (AS) in apolipoprotein E (ApoE) and low density lipoprotein receptor (LDLR) knockout mice (ApoE(-/-), LDLR(-/-)fed high-fat diet.

<b>METHODSb>Eight C57BL/6J mice fed with normal diet were used as control, 32 ApoE(-/-) mice and LDLR(-/-) mice were divided into normal diet and high-fat diet groups (n = 8 each). After 4 months, aorta was collected for morphologic (HE, Oil Red O, Von Kossa) and immunohistochemistry (nuclear factor-κB, IKB, macrophage surface molecule-3, α-smooth action protein) analysis.

<b>RESULTSb>Degree of AS in ApoE(-/-) and LDLR(-/-) mice fed with high-fat diet were significantly severer than those fed with normal diet and AS was more significant in ApoE(-/-) mice than in LDLR(-/-) mice. NFκB and IKB expressions in high-fat diet group were significantly higher than the normal diet group (P < 0.05). Double-labeling of NFκB revealed dominant expression in smooth muscle cells. Calcium deposition was significantly more in ApoE(-/-) mice fed with high-fat diet than mice fed with normal diet (P < 0.05) and was similar in LDLR(-/-) mice fed with high and normal diet (P > 0.05).

<b>CONCLUSIONb>High-fat diet contributes to the formation of AS plagues in ApoE(-/-) and LDLR(-/-) mice joined by upregulated NFκB and IKB expressions and calcium deposition.

Animals ; Apolipoproteins E ; genetics ; metabolism ; Calcium ; metabolism ; Female ; I-kappa B Proteins ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NF-kappa B ; metabolism ; Plaque, Atherosclerotic ; metabolism ; pathology ; Receptors, LDL ; genetics ; metabolism

<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