There are very tight interactions between the endocrine system and the liver. Hormones control many metabolic reactions and many processes of protein synthesis in the liver. The liver, on the other hand, is the major site for hormone metabolism. In the liver hormones may eitherbe transformed into more active compounds (e.g., thyroxine into the four times as active triidothyronine, vitamin 03 into its 25-0H form) or be inactivated, catabolized and disposed of. Liver also influences hormone blood levels, being the site of transport protein synthesis. It is also the major source of hormone-dependent growth factors and of their inhibitors. These complex interactions between hormones and liver occur via receptors. Accordingly, specific membrane, cytoplasmic, and nuclear receptors for many hormones have been identified in liver tissue [1]. The effectiveness of hormonal actions depends on the presence of specific receptors and is modulated by their concentration. The receptor binding capacity can be modified by the specific binding hormone and by other hormones as well. For example, estrogens may increase both estrogen and prolactin (PRL) receptors while testosterone decreases estrogen and PRL binding. Receptors for sexual hormones with properties similar to those in hormone-dependent sexual target tissues are present in the liver [2][3][4][5]. Very interesting studies carried out in the rat have shown sex-linked differences in some liver functions: there are differences in male and female steroid-metabolizing enzymes in the liver; male livers have more oxidizing enzymes and female livers have more reducing enzymes [6,7]; females have estrogen and PRL receptors; males, beside estrogen, have also androgen but not PRL receptors. Furthermore, male livers synthesize a malespecific protein -a male estrogen binder (MEBP) [3,7] which is not a receptor -and a protein excreted with the urine, the a-2u globulin [8]. These sex-linked differences are determined in the fetus at birth by androgen "imprinting" at the hypothalamic level, which represses a pituitary feminizing factor which has been identified as growth hormone [9]. Interestingly, growth hormone (GH) is secreted with a different pattern in male and female rats; this might be the signal which regulates the sexual dimorphism of these liver functions.Exogenous and endogenous estrogen excess (e.g., oral contraceptives and pregnancy) may effect several liver functions. It increases the synthesis of several proteins, such as hormone-transport proteins, ceruloplasmin, renin substrate, some drug-metabolizing enzymes, aminolevulinic acid synthetase, etc. Both estrogens and androgens seem to playa role in hepatic regeneration [10][11][12]. There is clinical evidence for an association between liver focal nodular hyperplasia and hepatocellular adenoma on one hand and oral contraceptive or anabolic steroid intake on the other [7,13]; elevated estrogenbinding capacity was found in liver adenoma tissue [14]. Hepatocellular carcinoma is
Assessment and Management or Hepatobiliary Diseas...