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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Decreased serum cholesterol-binding reserve in premature myocardial infarction.

Incubation of human serum with crystalline cholesterol which had been pulverised by sonication resulted in a measurable uptake of cholesterol by the serum. This uptake was designated "serum cholesterol-binding reserve" (S.C.B.R.). Among more than 200 men and women examined, S.C.B.R. values varied from less than 10 to over 200 mg/dl, while the values from repeated determinations on two individuals over several months varied within 24 mg/dl. S.C.B.R. could be attributed to two serum-lipoprotein subfractions--S.F.V. separated from very-low-density lipoprotein and S.F.H. from high-density lipoprotein, by gel filtration. Without further purification, S.F.V. solubilised 4-5 mg and S.F.H. solubilised 0-36 mg of additional cholesterol/mg of protein, while the remaining bulk of the lipoproteins lacked this property. It is proposed that S.F.V. and S.F.H. have physiological roles in retarding atherogenesis by removing cholesterol from the arterial intima and carrying it back to the circulating serum. Accordingly, individuals who have low S.C.B.R. values, being deficient in S.F.V. and S.F.H., are at higher risk for the development of atherosclerosis and coronary heart-disease. This hypothesis was tested by comparing S.C.B.R. values of patients with premature myocardial infarction with values of controls. The results indicated a trend of increasing S.C.B.R. values with increasing levels of serum cholesterol and triglycerides among the controls, but this trend was virtually lost among the patients. The S.C.B.R. values also were lower among patients than controls, and the difference was statistically significant between patients and controls with serum-cholesterol above 250 mg/dl or fasting serum-triglycerides above 160 mg/dl. These results are consistent with the proposed hypothesis.[1]


  1. Decreased serum cholesterol-binding reserve in premature myocardial infarction. Hsia, S.L., Chao, Y.S., Hennekens, C.H., Reader, W.B. Lancet (1975) [Pubmed]
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