1985 Volume 13 Issue 4 Pages 923-929
The observation of metabolic process in LDL formation from VLDL is one of important problems to elucidate lipoprotein metabolism with regard to atherosclerotic changes. The hydrolysis of VLDL triglyceride elicited by lipoprotein lipase is the most noticeable phenomenon in this metabolic process. Apolipoprotein C-III (apo C-III) has been shown to be an inhibitor of lipoprotein lipase activity in competition with apo C-II. This study was intended to clarify the significance of serum apolipoprotein C-III in cerebrovascular disorders by observing fasting serum apo C-III level in 41 infarct and 14 hemorrhagic patients who had stroke 3 months or more previously, and 68 healthy adults. Serum apo C-III level was determined by single radial immuno-diffusion method using agar plate containing specific anti-apo C-III serum. The mean values and standard deviations of serum apo C-III in 11 healthy adults aged 20 to 29 years and in 19 above 60 years were 6.8±1.3mg/dl and 6.6+1.0mg/dl respectively. The values in 41 infarct and 14 hemorrhagic patients were 8.6±2.7mg/dl and 8.1±3.1mg/dl. The level in infarct patients was significantly higher than the value of 6.6±2.3mg/dl in 37 age-matched healthy adults. In subjects with normal total cholesterol and triglyceride concentration, patients' apo C-III level was also higher significantly than the level in healthy adults. The level in patients with good functional capacity was high. In patients, apo C-III was directly proportional to total cholesterol, triglyceride apolipoprotein A-II and C-II, and apo C-III correlated positively with serum albumin and plasma antithrombin III.
The high level of apo C-III in normolipidemic patients detected in present study confirms usefulness of observation of apolipoprotein rather than that of serum lipids in the investigation of lipoprotein metabolism relating to atherosclerotic changes in cerebrovascular disorders. Some significant relations of this apolipoprotein to the indicators of lipoprotein metabolism adopted in this observation are easily understandable. While the relations between apo C-III, serum albumin, and plasma antithrombin III call our attention as new findings in the investigation of athero-thrombotic disorders. High albumin level elicits increase in blood filtrability, and antithrombin III inhibits clotting as well known.
Free fatty acids (FFA) liberated in the hydrolysis of VLDL triglyceride by the action of LPL binding with apo C complex is mostly conjugated with albumin, and non-conjugating FFA promotes thrombus formation. From these facts and high level of apo C-III in patients with good functional capacity, it is concluded that apo C-III regulates FFA liberation from VLDL triglyceride by competition with apo C-II, and inhibits following thrombus formation relating to the occurrence of ischemic lesion in the brain and heart.
