LIPOPROTEIN METABOLISM IN POSTMENOPAUSAL AND OOPHORECTOMIZED WOMEN

Objective: To investigate the mechanisms of accumulating cholesterol, and to analyze the metabolism of excess tissue cholesterol in women with low plasma levels of sex steroid hormones. Methods: We measured plasma concentrations of cholesterol, triglyceride, apolipoproteins, sex steroid hormones, and lecithin cholesterol acyltransferase activity in 20 premenopausal, ten postmenopausal, and ten bilaterally oophorectomized women. Lipoprotein lipase and hepatic triglyceride lipase activities were measured in postheparin plasma. We compared the three groups and evaluated a correlation between lipid metabolism and sex steroid hormone concentrations. Results: The mean plasma low-density lipoprotein (LDL) cholesterol level, lecithin cholesterol acyltransferase activity, and postheparin plasma lipoprotein lipase activity were higher in the postmenopausal and surgically menopausal groups. The mean plasma high-density lipoprotein (HDL) cholesterol concentration and postheparin plasma hepatic triglyceride lipase activity did not differ significantly among the three groups. The plasma LDL cholesterol level and postheparin plasma lipoprotein lipase activity showed a significantly negative correlation with plasma concentration of estrone (LDL: r = 0.64, P < .001; lipoprotein lipase: r = 0.54, P < .005) and estradiol (LDL: r = 0.65, P < .001; lipoprotein lipase: r = 0.47, P < .01), but not with that of testosterone. There was no significant relationship between postheparin plasma hepatic triglyceride lipase activity and plasma sex steroid hormones. Plasma lecithin cholesterol acyltransferase activity correlated significantly with plasma LDL cholesterol concentration, but not with levels of sex steroid hormones. Conclusion: Because of low endogenous estrogens, enhanced postheparin plasma lipoprotein lipase activity may lead to an elevated plasma LDL cholesterol concentration in postmenopausal and bilaterally oophorectomized women. We demonstrated an accelerated cholesterol esterification in HDL cholesterol that may have been induced by LDL cholesterol accumulation, although the HDL cholesterol concentration remained unchanged.