The immunoreactivity of apolipoprotein B (apo B) in plasma obtained from 238 unrelated black African male subjects from the People's Republic of Congo was analysed by non-competitive Enzyme Linked-Immunosorbent Assay (ELISA) with monoclonal BIP 45 anti-LDL antibody. The polymorphism detected by BIP 45 monoclonal antibody is identical to the Ag(c,g) polymorphism. Antibody BIP 45 distinguishes three apo B allotypes (immunophenotypes) encoded by the two allelic genes apo B Ag(c) and apo B Ag(g). Because of co-dominant transmission, genotypes may be inferred from allotypes, and it has been shown that BIP 45 binds strongly to the Ag(c) factor and only weakly to the allelic Ag(g) factor. Analysis of the Congolese plasma samples indicated that 67.65% of them bound BIP 45 with low affinity (Ag(c-,g+) genotype), 28.15% with intermediate affinity (Ag(c+,g+) genotype) and 4.20% with high affinity (Ag(c+,g-) genotype). According to the Hardy-Weinberg equilibrium, this corresponds to gene frequencies of 0.817 and 0.183 for the type Ag(g)/Ag(c) alleles, respectively. After adjustment for age and body-mass index, it was found that the Ag(c) allele decreases the apo B level by 9.62 mg/dl and that the Ag(g) allele increases apo B by 0.43 mg/dl. Therefore, as much as 4.30% of the genetic variance for apo B level could be accounted for by the Ag(c,g) gene locus.
Lipids, lipoproteins and apolipoproteins were analyzed in plasma of a city living Algerian population (Oran) free of obvious pathology. 129 individuals of this population were compared to a sample of subjects living in the surroundings of Lille (France). Several parameters were significantly different between the two populations. Cholesterol and phospholipids were lower in the population of Oran when compared with the population of Lille (4.90 mmol/l versus 5.47 mmol/l; 2.73 mmol/l versus 3.22 mmol/l respectively). Lipoproteins LpAI and LpAI:All were also lower in the population of Oran in comparison with the population of Lille (0.38 g/l versus 0.52 g/l; 0.68 g/l versus 1.00 g/l respectively), while LpCIII:B, LpE:B and Lp(a) were higher in the population of Oran when compared with the population of Lille (0.09 g/l versus 0.06 g/l; 0.28 g/l versus 0.16 g/l; 0.1 g/l versus 0.048 g/l) respectively. Several results argue in favor of the use of these lipoprotein parameters to better define the atherosclerotic risk. This was the main reason for characterizing the lipoprotein profile of such a population with a still unknown cardiovascular disease incidence.
Abstract A non competitive enzyme-linked immunosorbent assay (ELISA) for total apolipoprotein (apo) B, apo B with apo C-III (LpC-III:B), and apo B with apo E (LpE:B), was developed. Microtiter plates were used as solid-phase, and subdivided into three parts, coated respectively with affinity purified antibodies to apo B, to apo C-III and to apo E. After incubating the antigen with coated plates, a horseradish peroxidase-labelled antibody to apo B was added to all the plates to estimate total apo B, LpC-III:B and LpE:B. Key Words: Lipoprotein particlesELISAApo BLpC-III:BLpE:B.
Plasma lipids, lipoproteins, and lipoprotein[a] (Lp[a]) levels were determined in 216 members of 14 families with familial hypercholesterolemia (FH). Ninety-nine subjects harbored a mutant low density lipoprotein (LDL) receptor allele as confirmed by molecular genetic analysis. Four different mutant alleles were identified, each in a defined genetic group, Druze, Christian-Arabs, and Ashkenazi and Sephardic Jews. The findings in FH subjects (cases) were compared with their nonaffected family members (controls). Plasma Lp[a] levels increased with age in the controls but not in cases and were different among the four genetic groups. Mean plasma Lp[a] levels were significantly higher in cases (33 mg/dl) than in controls (22 mg/dl). Plasma LDL cholesterol levels were raised in cases of the four genetic groups to a similar extent, in contrast to the mean plasma Lp[a] that varied. The Lp[a] level was higher by 30-33% in cases from the Druze, Christian-Arabs, and Jewish-Ashkenazi groups but by 110% in the Jewish-Sephardic group. Apo[a] isoform distribution was similar in cases and controls within each genetic group. Lp[a] levels were highest in subjects with LpS1 isoform, in particular in cases from the Jewish-Sephardic group. These data indicate that the higher Lp[a] levels in FH heterozygotes cannot be attributed solely to lack of functional LDL receptor molecules but possibly reflect multiple gene interactions.
