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|Title:||Reproductive Endocrinology of Non-Alcoholic Fatty Liver Disease.|
|Authors:||Grossmann, Mathis;Wierman, Margaret E;Angus, Peter W;Handelsman, David J|
|Affiliation:||Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia|
Department of Medicine, University of Colorado Anschutz Medical Campus Aurora, CO, USA
Department of Gastroenterology and Hepatology, Austin Health, Heidelberg, Victoria, Australia
ANZAC Research Institute, University of Sydney, Concord Hospital, Sydney NSW, Australia..
Department of Endocrinology, Austin Health, Heidelberg, Victoria, Australia
Research Service, Rocky Mountain Regional Veterans Affairs Medical Center, Aurora CO, USA
|Citation:||Endocrine reviews 2018; online first: 30 November|
|Abstract:||The liver and the reproductive system interact in a multifaceted bidirectional fashion. Sex steroid signaling influences hepatic endobiotic and xenobiotic metabolism and contributes to the pathogenesis of functional and structural disorders of the liver. In turn, liver function impacts on the reproductive axis via modulating sex steroid metabolism and transport to tissues via sex hormone binding globulin (SHBG). The liver senses the body's metabolic status and adapts its energy homeostasis in a sex-dependent fashion, a dimorphism signaled by the sex steroid milieu and possibly related to the metabolic costs of reproduction.Sex steroids impact the pathogenesis of non-alcoholic fatty liver disease, including development of hepatic steatosis, fibrosis and carcinogenesis. Preclinical studies in male rodents demonstrate that androgens protect against hepatic steatosis and insulin resistance both via androgen receptor signaling and, following aromatisation to estradiol, estrogen receptor signaling, through regulating genes involved in hepatic lipogenesis and glucose metabolism. In female rodents in contrast to males, androgens promote hepatic steatosis and dysglycemia, while estradiol is similarly protective against liver disease.In men, hepatic steatosis is associated with modest reductions in circulating testosterone, in part consequent to a reduction in circulating SHBG. Testosterone treatment has not been demonstrated to improve hepatic steatosis in randomised controlled clinical trials. Consistent with sex-dimorphic preclinical findings, androgens promote hepatic steatosis and dysglycemia in women, whereas endogenous estradiol appears protective in both men and women. In both sexes, androgens promote hepatic fibrosis and the development of hepatocellular carcinoma, whereas estradiol is protective.|
|Appears in Collections:||Journal articles|
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