Abstract
The mammalian liver contains specific estrogen receptors (ERs) (DUFFY and DUFFY 1976; ATEN et al. 1978; ERIKSSON 1982a; ERIKSSON 1982b; FREYSCHUSS et al. 1991), but is still quite different from other target organs for estrogens. The number of binding sites in the liver is only about one-eighth to one-tenth that of the normal receptor concentration in classical target organs such as the uterus (ERIKSSON 1982a; ERIKSSON 1983). Liver receptors, in significant concentration, can only be detected after the onset of puberty and, in rats, hypophysectomy results in a major decrease of hepatic estrogen receptors (ERIKSSON 1983). Activation of the receptor is not associated with the induction of a progesterone receptor in the liver and, compared with the estradiol doses required to elicit response in the endometrium, excessively high doses are necessary to achieve similar effects in the liver (MARR et al. 1980; LAX et al. 1983). EAGON et al. (1986) have found a circadian rhythm in the hepatic ER, although we have not been able to repeat these findings (SAHLIN and FREYSCHUSS, unpublished observations).
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Sahlin, L., von Schoultz, B. (1999). Liver Inclusive Protein, Lipid and Carbohydrate Metabolism. In: Estrogens and Antiestrogens II. Handbook of Experimental Pharmacology, vol 135 / 2. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60107-1_8
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