The elevations of serum cholesterol of young volunteers who had taken daily 2500mg cholesterol in egg yolk for 14 days were varied individually. Some persons had marked elevations in their serum cholesterol as much as 70mg/100ml by the egg yolk intakes, whereas the others had no siginificant changes. As such human beings, there was a strain of rats whose serum cholesterol was easily increased by feeding of a high cholesterol diet. Their decay curves and biliary excretions of radioactivites from injected labeled cholesterol were decreased and cholesterol 7 α-hydroxylations in the livers were impaired when compared with normal rats. This defect of cholesterol metabolism was proved to be heritable for generations. From long term observations of the animals, it was found that the elevations of serum cholesterol of the rats in the course of aging were larger than those of controls. Although hepatic cholesterogenesis was markedly reduced in aged rat, the protein synthesis in beta-lipoprotein seemed to be unaffected. This discrepancy between lipid and protein synthesis in lipoprotein might have some influences on elevation of serum cholesterol level in the aged together with decrease of cholesterol catabolism. Therefore, genetic defects, dietary factors and aging must be particularly emphasized for the etiology of hypercholesterolemia. Actually, elevations of serum cholesterol by the egg yolk intakes in elder volunteers in their forties were higher than those of younger men.
Circulating serum beta-lipoprotein was influenced quantitatively and qualitatively by the oral administration of large amount of cholesterol. The increase of protein moiety of beta-lipoprotein was much less than that of cholesterol moiety. So, the amount of cholesterol per apoprotein had to increase by high cholesterol intake. On the other hand, content of triglyceride per apoprotein was rather decreased. The increase of protein synthesis in beta-lipoprotein by cholesterol ingestion was tranient and synthetic rate was not different from control after 1 week of cholesterol feeding. The turnover rate of labeled protein in beta-lipoprotein was not affected by hypercholesterolemia due to cholesterol ingestion, though turnover rate of cholesterol itself was accelerated.
Increase of protein synthesis in beta-lipoprotein by plasmapheresis or Triton injection induced the increase of hepatic cholesterogenesis.
As metabolism of lipoprotein and cholesterol have interfere with each others, we must consider the hypercholesterolemias from the view point of both factors.

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