The ovarian hormone deficiency-induced hypercholesterolemia is reversed by soy protein and the synthetic isoflavone, ipriflavone

The purpose of this study was to compare the effects of soy protein isolate with normal isoflavone content (soy) and with reduced isoflavone content (soy-), ipriflavone (IP), a synthetic isoflavone; and 17 beta-estradiol (E(2)) on lipid metabolism in ovariectomized (ovx) rats. Seventy-two 95-day old Sprague-Dawley rats were assigned to six groups: sham operated (sham), ovx, ovx+soy, ovx+soy-, ovx+IP, and ovx+E(2). Rats in the sham, ovx, ovx+IP, and ovx+E(2) groups were fed a casein-based diet, whereas the soy and soy- groups were fed diets in which casein was replaced with soy or soy-. Animals were pair-fed to the mean food intake of ovx+E(2) for 35 days. At the end of the study, animals were sacrificed in a nonfasted state and blood was collected via abdominal aorta. The ovx-induced increase in serum total cholesterol was reversed by all the treatments including ipriflavone and soy. Serum triglyceride levels were not significantly affected by any of the treatments. Liver cholesterol (mu mol/g) in animals receiving IP or fed soy were significantly (p<0.01) lower than the ovx, ovx+soy-, and ovx+E(2) groups. Liver lipids (mg/g) were significantly (p<0.05) lower in the animals that received E(2) or fed soy, but not those which were fed soy- or given IF. The ovx-induced increase in abdominal fat was completely reversed by soy and E(2) treatments but not by soy- or ipriflavone treatments. Soy, soy-, and IP had no uterotrophic activity as compared to E(2). Ovariectomy significantly increased body weight gains which were not suppressed by any of the treatments except E(2). These data indicate that ipriflavone is effective in preventing the unfavorable changes in serum and liver cholesterol associated with ovarian hormone deficiency in this animal model. Moreover, the consumption of synthetic or natural isoflavones may offer a potential alternative therapy in the treatment of hypercholesterolemia in ovarian hormone-deficient women. (C) 1997 Elsevier Science Inc.