Sex Hormone-Dependent Physiology and Diseases of Liver

Paulina Kur, Agnieszka Kolasa-Wołosiuk, Kamila Misiakiewicz-Has and Barbara Wiszniewska
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Paulina Kur: Department of Histology and Embryology, Faculty of Medicine and Dentistry, Pomeranian Medical University, Powst. Wlkp. 72, 70-111 Szczecin, Poland
Agnieszka Kolasa-Wołosiuk: Department of Histology and Embryology, Faculty of Medicine and Dentistry, Pomeranian Medical University, Powst. Wlkp. 72, 70-111 Szczecin, Poland
Kamila Misiakiewicz-Has: Department of Histology and Embryology, Faculty of Medicine and Dentistry, Pomeranian Medical University, Powst. Wlkp. 72, 70-111 Szczecin, Poland
Barbara Wiszniewska: Department of Histology and Embryology, Faculty of Medicine and Dentistry, Pomeranian Medical University, Powst. Wlkp. 72, 70-111 Szczecin, Poland

IJERPH, 2020, vol. 17, issue 8, 1-26

Abstract: Sexual dimorphism is associated not only with somatic and behavioral differences between men and women, but also with physiological differences reflected in organ metabolism. Genes regulated by sex hormones differ in expression in various tissues, which is especially important in the case of liver metabolism, with the liver being a target organ for sex hormones as its cells express estrogen receptors (ERs: ERα, also known as ESR1 or NR3A; ERβ; GPER (G protein-coupled ER, also known as GPR 30)) and the androgen receptor (AR) in both men and women. Differences in sex hormone levels and sex hormone-specific gene expression are mentioned as some of the main variations in causes of the incidence of hepatic diseases; for example, hepatocellular carcinoma (HCC) is more common in men, while women have an increased risk of autoimmune liver disease and show more acute liver failure symptoms in alcoholic liver disease. In non-alcoholic fatty liver disease (NAFLD), the distinction is less pronounced, but increased incidences are suggested among men and postmenopausal women, probably due to an increased tendency towards visceral fat accumulation.

Keywords: gender-dependent liver failure; hepatic glucose metabolism; insulin resistance; type 2 diabetes; metabolic syndrome; hepatic lipid metabolism; non-alcoholic fatty liver disease; cirrhosis; hepatocellular carcinoma; transgenic animal models; clinical cases (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2020
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