The inheritance of sinking-pre-beta lipoprotein and its relation to the Lp(a) antigen.
We have investigated the genetics of plasma sinking-pre-beta lipoprotein (sp beta) as determined by the method of Breckenridge and Maguire, using several approaches: (i) a population study, (ii) a twin study and (iii) the use of family data. In addition, by the use of split samples, the sp beta level as determined by us was correlated with Lp(a) typing carried out in Oslo by Dr. Kåre Berg. Although the sp beta level is a continuous character, the results clearly showed it to be to a considerable extent under the control of the major autosomal gene pair constituted by the alleles Lpa and Lp, which mainly control the production of the Lp(a) antigen, Lpa being dominant. In our data the boundary between the LpLp and LpaLp genotypes appeared to fall between the sp beta 2 and 3 mg% levels, while that between LpaLp and LpaLpa was in the 15 mg% region. These boundaries, which were inferred from both typing and population statistics, received good confirmation from the family data. It appears that some 88% of the variation in sp beta level is directly ascribed to segregation of Lpa and Lp. On the basis of the twin study and other data, we conclude that the residual observed variation in sp beta is almost entirely ascribed to analytical error of determination and polygenic effects, the influence of environment being negligible. The heritability is close to 100%.
D000941:Antigens / Q000235:genetics*; D002869:Chromosome Aberrations; D025063:Chromosome Disorders; D003241:Consanguinity; D005260:Female; D006801:Humans; D008079:Lipoproteins, VLDL / Q000097:blood / Q000235:genetics*; D008297:Male; D011247:Pregnancy; D014427:Twins
D000941:Antigens; D008079:Lipoproteins, VLDL