The effects of acquired obesity on lipid profile and lipoprotein composition in rare BMI-discordant monozygotic (MZ) twin pairs were studied.
Abdominal fat distribution, liver fat (magnetic resonance imaging and spectroscopy), fasting serum lipid profile (ultracentrifugation, gradient gel-electrophoresis, and colorimetric enzymatic methods), and lifestyle factors (questionnaires and diaries) were assessed in 15 BMI-discordant (within-pair difference [?] in BMI >3 kg/m2) and nin concordant (?BMI
The offspring of individuals with a history of premature myocardial infarction are at increased risk of premature coronary attacks. The aim of this study was to determine parent/offspring associations of coronary risk factors in families affected by premature myocardial infarction and to compare these to corresponding control families.
The cohort of cases consisted of 71 male survivors of myocardial infarction and their 128 descendants (aged 7-18 years). As control families, 85 randomly selected healthy males with their 66 descendants were investigated. Besides traditional risk factors, serum high sensitive C-reactive protein (hsCRP), apolipoprotein (apo) E phenotypes and lipoprotein(a) were analyzed.
In the offspring of the patients, fibrinogen and atherogenic lipoprotein parameters were higher than in the corresponding controls, but hsCRP, lipoprotein(a) and anthropometric data did not differ between the groups. The adult-offspring positive correlations were detected in fibrinogen and in almost all measured lipoprotein fractions in the affected families; amongst the controls, the association was observed only for triglyceride levels. Multiple logistic regression analysis demonstrated independent association of offspring apoB, apoA-I and fibrinogen levels with a family history of premature myocardial infarction.
The most informative predictors of future coronary attacks during childhood are apoB-100 and apoB/apoA-I ratio; serum hsCRP and lipoprotein(a) do not have predictive value in childhood.
BACKGROUND: Alimentary lipemia has been associated with coronary heart disease and common carotid artery intima-media thickness (IMT). This study was designed to investigate the relations of subclasses of postprandial triglyceride-rich lipoproteins (TRLs) with IMT. METHODS AND RESULTS: Ninety-six healthy 50-year-old men with an apolipoprotein (apo) E3/E3 genotype underwent an oral fat tolerance test and B-mode carotid ultrasound examination. The apo B-48 and apo B-100 contents of each fraction of TRLs were determined as a measure of chylomicron remnant and VLDL particle concentrations. In the fasting state, LDL cholesterol (P
The net mass transfer (NMT) of cholesteryl esters (CEs), triglycerides (TGs), and phospholipids (PLs) between lipoproteins was measured after incubation of fresh plasma for up to 2 hours from 18 male alcohol abusers and 17 male volunteer control subjects. In alcohol abusers the mean value of CE NMT was 3.7 nmol.mL-1.h-1 from apolipoprotein B-containing lipoproteins (apoB-containing lipoproteins) to HDL and in control subjects 8.7 nmol.mL-1.h-1 from HDL to apoB-containing lipoproteins. The NMT of PL was higher in alcohol abusers than in control subjects (35.0 vs 11.6 nmol.mL-1.h-1 from apoB-containing lipoproteins to HDL, respectively), and plasma PL transfer protein (TP) activity was 33% higher (P
The EcoR1 polymorphism of the apolipoprotein B gene (APOB) is thought to be associated with atherothrombotic type of ischemic stroke (ATTIS) with the APOB*R1/R2 genotype as a marker of increased risk for ATTIS. We estimated odds ratio for this genotype as 2.17 in ethnic Russians and 3.39 in ethnic Tartars. The association between the EcoR1 APOB gene polymorphism and ATTIS confirmed the results of previous studies on relation of the APOB gene to vascular pathology caused by elevated lipid level and atherogenesis.
The insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene has been postulated to be associated with CAD in some populations of European descent. As part of a study investigating metabolic and genetic factors in subjects with premature coronary artery disease (CAD), we examined the I/D polymorphism of the ACE gene in 134 subjects with premature CAD (105 men and 29 women, mean age 49 +/- 6 years) and 116 control subjects selected for health (71 men, 45 women; mean age 39 +/- 7 years). Both patients and controls were of French Canadian descent. As expected, significant differences were found between cases and controls with respect to age, plasma lipoprotein cholesterol, presence of smoking, diabetes and high blood pressure after correction for age. Multivariate analysis confirms the importance of age, HDL-C levels, smoking and apo B levels as determinants of CAD. Allele frequencies of the I and D polymorphism were 43.1% and 57.9% in controls, and 48.5% and 51.5% in CAD cases (chi 2 = 0.622, p = 0.430). No significant association between the I/D polymorphism and conventional cardiovascular risk factors, including plasma levels of lipids, lipoprotein cholesterol, diabetes or smoking, was found in cases or controls. Furthermore, the presence of the I/D polymorphism did not correlate with a history of hypertension or a family history of premature CAD in CAD patients. We conclude that, in our selected population, the I/D polymorphism of the ACE gene is not associated with CAD, conventional risk factors, or a family history of CAD. Although our sample size does not allow sufficient power to ascertain that the ACE I/D polymorphism is not associated with CAD, we do not recommend the routine measurement of the ACE polymorphism in our population to determine cardiovascular risk.
(i) To estimate changes in apoB and apoB/apoA-I, reflecting the balance between atherogenic and anti-atherogenic lipoprotein particles, by exercise training and compare with changes in LDL-C and TC/HDL-C ratio, and (ii) To compare strengths of relationships between physical fitness and various lipoprotein variables.
The study was a 1-year open randomized trial comprising 219 healthy middle-aged subjects aged 40-49 years who were allocated to exercise or no exercise, dietary advice or no advice in a 2 x 2 factorial design. This study includes 188 men who completed the trial, 45 to diet, 48 to exercise, 58 to diet + exercise and 37 to control.
Exercise; supervised endurance exercise three times a week. Diet; reduce weight, increase intake of fish and reduce total fat intake.
One-year change in apoB and apoB/apoA-I ratio.
Exercisers decreased their ApoB and ApoB/ApoA-I values significantly compared to non-exercisers. LDL-C was not, but LDL-C/HDL-C was marginally but statistically significantly reduced by exercise. One-year change in ApoB and ApoB/ApoA-I correlated more strongly to 1-year changes in physical fitness than LDL-C or LDL-C/HDL-C. Adjusting for changes in LDL-C or LDL-C/HDL-C did not influence the correlation between changes in fitness and ApoB or ApoB/ApoA-I. However, adjusting for changes in ApoB or ApoB/ApoA-I wiped out the correlation between change in fitness and LDL-C or LDL-C/HDL-C. Relationships weakened when adjusting for changes in waist circumference, but Apo B or ApoB/ApoA-I still correlated significantly to changes in fitness.
Physical exercise reduced the atherogenic burden as experienced by the reduction in apoB or apoB/apoA-I levels, but not by LDL-C in healthy middle-aged men. Possibly, regular physical activity might increase the LDL-C particle size, thereby making LDL less atherogenic. Monitoring of apolipoproteins rather than the cholesterol moiety of lipoproteins might improve the assessment of lipoprotein changes after exercise training.
In addition to traditional measurements of serum lipid levels, apolipoprotein A-I (apoA-I), apolipoprotein B (apoB), and apoB/apoA-I ratio may add more value to risk assessment guidelines for cardiovascular disease.
We calculated reference intervals for apoA-I, apoB, and apoB/apoA-I ratio using a reference sample (n=2828) from the FINRISK 2007 study.
The reference intervals for apoA-I were 1.1-2.0 g/l for men and 1.2-2.3 g/l for women. The corresponding reference intervals for apoB were 0.6-1.5 g/l and 0.6-1.3 g/l. The reference intervals for apoB/apoA-I ratio were 0.3-1.0 for men and 0.3-0.8 for women. Compared with the healthy reference group, obese men had the lowest ApoA-I, the highest apoB, and the highest apoB/apoA-I ratio. Men with CVD and cholesterol-lowering medication, or diabetes had lower apoB levels and apoB/apoA-1 ratio than the reference group but the opposite was true for women. The therapeutic goal for low-risk individuals for apoB was 0.9 g/l coinciding with LDL-C concentration of 3.0 mmol/l.
Reference intervals for apoA-I, apoB, and the apoB/apoA-I ratio and their cutoff values may be useful for the risk evaluation and follow-up of treatment among individuals having CVD or other metabolic disorders.
The apolipoprotein (apo) A-I:B ratio and the apo B concentration were determined by radial immunodiffusion in dried blood spot samples from 1,767 10- and 11-year-old children. Children with either apo A-I:B ratios below the first percentile or apo B levels above the 99th were recalled and plasma lipid and apolipoprotein profiles were determined for both children and parents. Of 17 children (one family was lost to follow-up) recalled due to abnormal apo A-I:B ratios, apo B levels were above the 95th percentile in 13 children, and of 18 children with abnormal apo B screening levels (three of them also had abnormal apo A-I:B ratios), the plasma apo B level was elevated in 13 children. The 23 children with abnormal blood lipid and/or apolipoprotein concentrations were divided into two main groups: (a) children with type IIa hyperlipoproteinemia and (b) children with hyperapo B lipoproteinemia (hyperapo B) and normal blood lipid levels. Twelve children had the type IIa pattern. Five children likely had familial hypercholesterolemia (FH), the other seven children may have hypercholesterolemia due to obesity or environmental factors. Eleven children had the hyperapo B abnormality. In four children, the elevated apo B level probably was an indication of the occurrence of familial combined hypercholesterolemia (FCH) in the family. Of the remaining seven hyperapo B children, three children also had a parent with hyperapo B and a fourth family suffered from obesity.(ABSTRACT TRUNCATED AT 250 WORDS)
Apolipoprotein A-IV (apoA-IV) is a glycoprotein constituent of triglyceride-rich and high-density lipoproteins (HDL) and may thus play an important role in lipid metabolism. In Finland two common isoforms (A-IV-1 and A-IV-2) of apoA-IV have been found. The isoforms are the result of the G to T substitution in the third base of the codon 360 in the apoA-IV-2 allele of the apoA-IV gene. The purpose of the study was to determine the apoA-IV allele frequencies in the Saami and the Finns, and to relate the apoA-IV phenotypes to serum lipids. The sample was drawn in connection with a Reindeer Herders' Health Survey performed in northern Finland in 1989. The study group included 248 men with known ethnic origin, Saami and Finns, who lived in the area of the nine northernmost municipalities of Finland. ApoA-IV phenotypes from 71 Saami (both parents Saami) and 177 Finns (both parents Finns) were determined by isoelectric focusing and Western blotting. Serum lipids were determined enzymatically. ApoA-IV allele frequencies in the Saami and the Finns were for A-IV-1 0.894 vs 0.944 and for A-IV-2 0.106 vs 0.056, respectively (chi2-test, P