Although the relationship between serum cholesterol and the pathogenesis of atherosclerosis has not been definitely established, it has been widely investigated. The bulk of the evidence favors an etiologic association between hypercholesteremia and atherosclerosis; both may be the end-products of an altered metabolic state. Because of this possibility, many therapeutic attempts have been made to lower serum cholesterol.
The serum cholesterol concentration in normal persons is approximately 37% of the total lipid content of the blood.1 The range is 190 to 250 mg. per 100 ml. of serum. Approximately 30% of the total cholesterol is in the free state and 70% in the form of cholesterol esters.2 The biosynthesis of cholesterol from acetate3 is thought to proceed as indicated in Figure 1.
Acetyl coenzyme A (CoA) condenses to form acetoacetyl CoA, which with the addition of one more acetyl CoA and a decarboxylation produces dimethylacrylate, which is a five-carbon unit.
OAKS W, LISAN P, MOYER JM. Inhibition of Cholesterol Synthesis with the Use of Mer-29. AMA Arch Intern Med. 1959;104(4):527–531. doi:10.1001/archinte.1959.00270100013003
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