Gynecomastia in 8 and testicular atrophy in all of the cases prompted us to investigate the sex hormone metabolism in addition to the usual clinical studies in these men. We are reporting here the results of urinary bioassays in these, as well as in a significant number of control subjects, including one case of subacute liver cirrhosis. Detailed clinical and postmortem dataof patients who died of liver failure will be reported elsewhere. Our preliminary report 1 last year suggested that estrogen metabolism was im-paired in advanced cirrhosis of the liver. The present data supplement and confirm our previous findings and also provide a theoretical basis for a hormonal etiology of gynecomastia in chronic liver disease. Since Zondek 2 enunciated the theory that the liver inactivates sex hormones, ample experimental proof of such a mechanism has been brought forward by a num-ber of workers 3—7.
Sex Hormone-Dependent Physiology and Diseases of Liver
This test measures the level of sex hormone binding globulin SHBG in your blood. SHBG is a protein made by your liver. It binds tightly to three sex hormones found in both men and women. These hormones are estrogen; dihydrotestosterone DHT , and testosterone. SHBG carries these three hormones throughout your blood. Although SHBG binds three hormones, the hormone that's critical in this test is testosterone. SHBG controls the amount of testosterone that your body tissues can use.
Sex dictates liver disease risk in hepatitis B
Sun J, et al. PLoS One. Men with hepatitis B are at increased risk for severe liver disease compared with women; however, lifestyle and environmental related exposures cannot explain the sex differences, suggesting biological causes, according to data published in PLoS One. Researchers examined whether lifestyle and environmental related exposures impacted the differences in liver disease severity observed between men and women infected with hepatitis B.
The liver is one of the most essential organs involved in the regulation of energy homeostasis. Hepatic steatosis, a major manifestation of metabolic syndrome, is associated with imbalance between lipid formation and breakdown, glucose production and catabolism, and cholesterol synthesis and secretion. Epidemiological studies show sex difference in the prevalence in fatty liver disease and suggest that sex hormones may play vital roles in regulating hepatic steatosis. In this review, we summarize current literature and discuss the role of estrogens and androgens and the mechanisms through which estrogen receptors and androgen receptors regulate lipid and glucose metabolism in the liver.