Hypolipidemic action of the soybean isoflavones genistein and genistin in glomerulonephritic rats

Effects of genistein and its glycoside genistin were studied in nephritic rats with endogenous hyperlipidemia. Male Wistar rats with glomerulonephritis caused by a single intravenous injection of nephrotoxic serum were orally given 5 mg of genistein or 8 mg of genistin/d/100 g body weight for 12 d. These isoflavones suppressed nephritis-induced severe hypercholesterolemia and hypertriglyceridemia, and their hypolipidemic action was almost identical. Fecal steroid excretion was unchanged by administration of the two isoflavones. Genistein inhibited the incorporation of [1-14C]acetate into cholesterol and FA in liver slices from nephritic rats when added to an incubation buffer, whereas genistin did not. These results suggest that genistin may be hydrolyzed to genistein and that genistein itself and/or its metabolite(s) may be intracorporal entities suppressing hepatic lipid syntheses. They also suggest that the suppression of hepatic lipid synthesis may be one mechanism of the hypolipidemic action of genistein.