Moderate hyperalphalipoproteinaemia in a Brazilian population is related to lipoprotein lipase activity, apolipoprotein A-I concentration, age and body mass index (original) (raw)
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Metabolism, 1992
Familial Hypercholesterolemia (FH) is a condition characterized by markedly elevated blood cholesterol, low-density lipoproteins (LDL), and apolipoprotein B-100 (apo B). The molecular basis of this monogenie disease is the defective functioning of the cellular receptor for LDL that recognizes apo B. Lipoprotein(a) [Lp(a)] is a circulating lipoprotein that is structurally related to LDL, as it also contains apo B. To assess the impact of the LDL receptor deficiency on the plasma Lp(a) concentration, we measured Lp(a) in 28 FH patients and in 31 unaffected relatives. Because elevation of Lp(a) concentration in plasma of patients with coronary artery disease (CAD) appears to occur independently from plasma cholesterol levels, to avoid potentially confounding problems, members of the families chosen had no history for the disease. Whereas apo B clearly showed a bimodality of distribution by being significantly higher in the FH patients (188 2 38 mg/dL) than in the unaffected relatives (82 f 18 mg/dL), Lp(a) concentration did not differ in the two groups of patients (30 2 24 mg/dL in the FH patients Y 31 + 23 in the normolipidemic relatives). Similar results were obtained when only siblings were further considered. We conclude that although Lp(a) is closely related to LDL structurally, its level in plasma is not significantly affected by the LDL receptor activity.
Journal of Atherosclerosis and Thrombosis
The official journal of the Japan Atherosclerosis Society and the Asian Pacific Society of Atherosclerosis and Vascular Diseases Original Article Aims: Lipoprotein(a) [Lp(a)] is a plasma lipoprotein consisting of a low-density lipoprotein (LDL)-like particle with apolipoprotein (Apo)(a), attached via a disulfide bond to Apo B100. Previous studies have shown that high Lp(a) levels are associated with an increased risk of cardiovascular disease in patients with familial hypercholesterolemia (FH). To date, limited data are available as to distribution of Lp(a) in FH and associations of Lp(a) with other lipid profiles and cardiovascular disease. Our study aimed to investigate serum Lp(a) levels in relation to other lipid profiles and clinical conditions in the national largest-ever cohort of Japanese FH patients. Methods: This study is a secondary analysis of the Familial Hypercholesterolemia Expert Forum (FAME) Study that includes a Japanese nationwide cohort of FH patients. In 399 patients under treatment for heterozygous FH who had a baseline measurement of serum Lp(a), the present study examined the distribution of Lp(a) levels and associations of Lp(a) with other lipid profiles and clinical conditions including coronary artery disease (CAD). Results: The distribution of Lp(a) was skewed to the right with a median of 20.8 mg/dL, showing a log-normal distribution. Serum Apo B and Apo E levels were positively associated with Lp(a) levels. Age-adjusted mean of Apo B was 8.77 mg/dL higher and that of Apo E was 0.39 mg/dL higher in the highest category (40+ mg/dL) of Lp(a) than in the lowest category (20 mg/dL). LDL-C levels did not show such an association with Lp(a) levels. A tendency towards a positive relationship between Lp(a) and prevalent CAD was observed in men. Conclusion: Our study demonstrated a distribution pattern of Lp(a) in Japanese FH patients and positive relationships of Lp(a) with Apo B and Apo E levels. consisting of a low-density lipoprotein (LDL)-like particle with one additional protein, apolipoprotein(a), attached via a disulfide bond to apolipoprotein B100 1) .
Journal of lipid research, 1999
The metabolic and genetic determinants of HDL cholesterol (HDL-C) levels and HDL turnover were studied in 36 normolipidemic female subjects on a whole-food low-fat metabolic diet. Lipid, lipoprotein, and apolipoprotein levels, lipoprotein size, and apolipoprotein turnover parameters were determined, as were genetic variation at one site in the hepatic lipase promoter and six sites in the apolipoprotein AI/CIII/AIV gene cluster. Menopause had no significant effect on HDL-C or turnover. Stepwise multiple regression analysis revealed that HDL-C was most strongly correlated with HDL size, apolipoprotein A-II (apoA-II), and apolipoprotein A-I (apoA-I) levels, which together could account for 90% of the variation in HDL-C. HDL size was inversely correlated with triglycerides, body mass index, and hepatic lipase activity, which together accounted for 82% of the variation in HDL size. The hepatic lipase promoter genotype had a strong effect on hepatic lipase activity and could account for 3...
Atherosclerosis, 2011
Objective: Familial hypercholesterolemia (FH) is caused by defects in genes coding for proteins involved in low density lipoprotein (LDL) metabolism, and is associated with increased risk of premature coronary heart disease (CHD). The clinical phenotype of FH exhibits marked variability due to additional metabolic and environmental factors, and further biomarkers are required for appropriate risk assessment. The aim of the present study was to search for risk markers among FH patients. Methods and results: Clinical and biochemical parameters of FH subjects with early CHD events (CHDsusceptible) and FH subjects with late or no CHD events (CHD-resistant) were compared. Our data show that CHD-susceptible FH patients had significantly higher Lipoprotein (Lp) (a) levels compared to CHDresistant FH patients. When subdividing by gender, the main findings were that (i) CHD-susceptible women had significantly higher levels of both Lp(a), low density lipoprotein (LDL) cholesterol and apolipoprotein (apo) B as compared to CHD-resistant women, and (ii) CHD-resistant women had significantly lower Lp(a) levels and higher high density lipoprotein (HDL) cholesterol and apoA-I levels compared to CHD-resistant men. Conclusions: The data suggest that Lp(a) may be an important coronary risk marker in FH patients, in particular in combination with elevated LDL cholesterol levels among female subjects. Thus, measurement of Lp(a) levels may help identifying high-risk individuals who could benefit from an aggressive therapy, including statins to reduce LDL-cholesterol to guideline-recommended levels.
Human Genetics, 1994
We have tested for evidence of linkage between the genetic loci determining concentrations and composition of plasma high density lipoproteins (HDL) with the genes for the major apolipoproteins and enzymes participating in lipoprotein metabolism. These genes include those encoding various apolipoproteins (apo), including apoA-I, apoA-II, apoA-IV, apoB, apoC-I, apoC-II, apoC-III, apoE, and apo(a), cholesteryl ester transfer protein (CETP), HDL-binding protein, lipoprotein lipase, and the low density lipoprotein (LDL) receptor. Polymorphisms of these genes, and nearby highly polymorphic simple sequence repeat markers, were examined by quantitative sib-pair linkage analysis in 30 coronary artery disease families consisting of a total of 366 individuals. Evidence for linkage was observed between a marker locus D16S313 linked to the CETP locus and a locus determining plasma HDL-cholesterol concentration (P = 0.002), and the genetic locus for apoA-II and a locus determining the levels of the major apolipoproteins of HDL, apoA-I and apoA-II (P = 0.009 and 0.02, respectively). HDL level was also influenced by the variation at the apo(a) locus on chromosome 6 (P = 0.02). Thus, these data indicate the simultaneous involvement of at least two different genetic loci in the determination of the levels of HDL and its associated lipoproteins.
Bangladesh Journal of Medical Science, 2017
Background and rationale: HDL cholesterol is one of the 5 major groups of lipoproteins cholesterol, which enable lipids like cholesterol and TG to be transported within the water based blood stream. In healthy persons, about thirty percent of blood cholesterol is carried by HDL cholesterol. HDL-C is a potent predictor of coronary heart disease. Genetic as well as environmental factors including lifestyle factors play a role as determinants of its level in the blood. To examine the effects of certain lifestyle factors on serum level of high density lipoprotein cholesterol in young adult people HDL cholesterol seems to protect against CVD which increases the risk for heart disease. Subjects and methods: Three hundred and twenty five young adult subjects of both sexes aged 18-45 years asymptomatic for cardiovascular diseases were interviewed according to special questionnaire including information on lifestyle habits. Physical examination was done, height, body weight, and blood pressure measurements were performed. Blood analysis to determine the blood level of high density lipoprotein cholesterol was done after 12 hours fasting. Results and conclusion: Smoking and obesity were the most significant risk factors associated with a decreased level of high density lipoprotein cholesterol. The level of HDL-C was 50.5±11.5 mg/dl in smokers compared with 57.7±12.5 mg/dl in nonsmokers. Its level was 48.5 ±8.5 mg/dl in obese individuals compared to 57.5±11.7mg/dl in normal body weight subjects. Physical activity was not significantly associated with low level of HDL-C analysis, but it was found to be significantly associated with its level by the multiple regression analysis. High-density lipoprotein cholesterol level was a function of many factors, some of them were lifestyle related such as smoking, physical activity, and obesity. Therefore, efforts to encourage more physical activity, quitting smoking, consuming low fat diet, and keeping ideal body weight are recommended.