Estrogen-Induced Small Low-Density Lipoprotein Particles in Postmenopausal Women

Abstract

Objective: To investigate the mechanisms of an estrogen-induced decrease in the size of low-density lipoprotein (LDL) particles in postmenopausal women. Methods: Twenty postmenopausal women were treated with conjugated equine estrogen, 0.625 mg daily, for 3 months. Plasma levels of total cholesterol, triglyceride, high-density lipoprotein (HDL) cholesterol, and apolipoproteins AI, AII, and B were measured before and after therapy. We analyzed total, free, and esterified cholesterol, triglyceride, phospholipid, and apolipoprotein B levels in the LDL. Cholesterol, triglyceride, and phospholipid concentrations were measured by enzymatic methods. Apolipoprotein AI, AII, and B levels were determined by immunoturbidimetric assay. The diameter of LDL particles was determined by gradient gel electrophoresis. Results: Estrogen reduced significantly the plasma levels of total cholesterol and apolipoprotein B and increased significantly the plasma levels of triglyceride, HDL cholesterol, and apolipoproteins AI and AII. The ratio of cholesteryl ester to apolipoprotein B was significantly reduced, whereas the ratio of triglyceride to apolipoprotein B was significantly increased after such treatment. The plasma level of triglyceride showed a positive correlation with the ratio of LDL-triglyceride/apolipoprotein B ( r = .40, P < .01), and a negative correlation with the ratio of LDL-cholesteryl ester/apolipoprotein B ( r = −.55, P < .001). Estrogen treatment reduced significantly the diameter of LDL particles (25.79 ± 1.13 nm versus 24.94 ± 1.02 nm, P < .001). The diameter of the LDL particle was correlated negatively with the plasma level of triglyceride ( r = −.84, P < .001) and the ratio of LDL-triglyceride/apolipoprotein B ( r = −.58, P < .001), and positively with the ratio of LDL-cholesteryl ester/apolipoprotein B ( r = .57, P < .001). Conclusion: The results of this study indicate that an increase in the triglyceride plasma level induced by estrogen therapy appeared to produce small triglyceride-rich and cholesteryl ester–poor LDL particles that were of small size.