17-BETA-ESTRADIOL TREATMENT INCREASES THE LEVELS OF ESTROGEN-RECEPTORAND ITS MESSENGER-RNA IN MALE-RAT LIVER

This study examined estrogen receptor dynamics in the livers of male o bese rats (SHHF/Mcc-cp) treated for two weeks with a continuous, low d ose of 17 beta-estradiol compared with untreated controls. An increase d binding capacity for tritiated 17 beta-estradiol in the cytosol, con sistent with binding to the estrogen receptor, was demonstrated in tre ated males relative to control males (P < 0.01). These observations we re confirmed using curve-peeling techniques with saturation analysis, ammonium sulfate precipitation/fractionation of cytosol protein, and c hromatographic techniques to isolate the high-affinity binding from ot her interfering factors. Increased hepatic nuclear estrogen receptor l evels in treated males (112.3 +/- 8.3 fmol/g liver) compared with cont rols (64.1 +/- 6.8 fmol/g liver) suggested that the liver was under es trogenic influences. This interpretation was supported by an increase in serum triglyceride levels, reflecting increased very low density li poprotein secretion by the liver. Reductions in testosterone levels an d in the weights of seminal vesicles and the testes in treated males i ndicated detrimental effects on reproduction. An interpretation of inc reased synthesis of estrogen receptor with 17 beta-estradiol treatment was supported by the observation of an increase in the mRNA for estro gen receptor. Taken together, these observations indicate that continu ous, low-dose 17 beta-estradiol treatment induces estrogenic action in the livers of male rats and also increases hepatic estrogen receptor, probably indirectly, via increase in its mRNA.