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Plasma apolipoprotein CII levels in hypertriglyceridemia
Insights
Hypertriglyceridemia is linked to increased plasma apolipoprotein CII (apoCII). A strong correlation exists between apoCII and triglycerides (TG), supporting a lipoprotein structural model.
Area of Science:
- Lipid Metabolism
- Cardiovascular Research
- Biochemistry
Background:
- Hypertriglyceridemia is associated with elevated plasma apolipoprotein CII (apoCII).
- Understanding the relationship between triglycerides (TG) and apoCII is crucial for lipid metabolism research.
Purpose of the Study:
- To investigate the quantitative relationship between plasma apoCII and TG levels in hypertriglyceridemic patients.
- To assess the validity of a lipoprotein structural model in explaining this relationship.
Main Methods:
- Examined 30 hypertriglyceridemic patients (types I, IV, V HL) and 10 controls.
- Measured plasma apoCII using single radial immunodiffusion.
- Analyzed the correlation between the square roots of apoCII and TG values.
Main Results:
- A significant positive correlation (r = .95, P < 0.001) was found between the square root of apoCII and the square root of TG.
- The regression line indicated a strong relationship: sqrt(apoCII) = 0.37 * sqrt(TG) - 0.03.
- Type I hyperlipoproteinemia patients showed apoCII levels comparable to their TG levels, differing from previous reports.
Conclusions:
- A lipoprotein structural model effectively explains the observed relationship between apoCII and TG.
- The findings suggest that apoCII levels in hypertriglyceridemia are primarily determined by TG-rich lipoproteins.
- The study provides insights into apoCII regulation in different types of hyperlipoproteinemia.
Abstract:
It is known that hypertriglyceridemia is associated with the elevation of plasma apolipoprotein CII (apoCII). In an attempt to look at the relationship between the two, the present study was conducted. We examined 30 patients with hypertriglyceridemia (TG, 210 to 9,127 mg/dL) and ten normolipidemic controls. Hypertriglyceridemic patients included 7 of type I hyperlipoproteinemia (HL), 17 of type IV, and 6 of type V. Plasma apoCII was measured by the single radial immunodiffusion method. Major cause for any difference in plasma apoCII could be attributed to differences in the TG-rich lipoproteins. Since a model for the lipoprotein structure indicates that TG-rich lipoproteins are spherical, with apoCII as a surface component and TG as a core substance, we calculated the square roots and the cubic roots of the values of apoCII and TG to make comparison possible. When the two variables were plotted on the X and Y axes respectively, we obtained the regression line of square root of apoCII = 0.37 X 3 the square root of TG - 0.03 with a correlation coefficient of r = .95 (P less than 0.001). The result indicates that a lipoprotein structural model accounts well for the relationship between apoCII and TG. Although a previous report suggested a compensatory increase of apoCII in lipoprotein lipase deficiency, our patients with type I HL had apoCII levels similar to those who had comparable levels of plasma TG.