Preventive Female Sex Factors Against The Development of Chronic Liver Disease

Non-Alcoholic Fatty Liver Disease in Females and Males

Author(s): Yosho Fukita, Tsutoshi Asaki, Yoshiki Katakura, Ichiro Shimizu

Pp: 94-106 (13)

DOI: 10.2174/978160805293611201010094

* (Excluding Mailing and Handling)


Increasing evidence indicates that hepatic fat accumulation is related to hepatic fibrosis, inflammation, apoptosis, and cancer. Males generally have larger visceral fat areas than females. Menopause is associated with a shift towards relatively more fat as well as towards the deposition of more fat in the abdominal region. Estrogen treatment of male-to-female transsexuals can increase the amount of subcutaneous adipose tissue; thus, estrogen changes the male type of visceral fat distribution into a female type of fat accumulation. Visceral fat accumulation arises through enlarged adipocytes, which release adiponectin, leptin, tumor necrosis factor-α (TNF-α), and fatty acids. Adiponectin inhibits the enlargement of adipocytes and fat accumulation. Adiponectin levels are consistently higher in females than in males. Persistent TNF-α stimuli lead to adipogenesis and impairment of mitochondria in hepatocytes and result in induction of oxidative stress. In experimental studies, when incubated with adiponectin, hepatic stellate cells undergo a number of antifibrogenic changes. Whereas leptin may play a role in the development of hepatic fibrosis. Hepatic steatosis spontaneously becomes evident in an aromatase-deficient mouse. Estrogen replacement reduces hepatic steatosis and restores the impairment in mitochondrial fatty acid β-oxidation to a wild-type level. In fact, tamoxifen, as an antiestrogen, has been shown to be associated with an increased risk of developing hepatic steatosis and non-alcoholic steatohepatitis (NASH) in non-obese female patients with breast cancer.< /p> < p>Understanding the sex-associated difference is necessary to inform the rational design of treatment strategies directed at visceral obese individuals who may develop from hepatic steatosis to cirrhosis and hepatocellular carcinoma.

Keywords: Non-alcoholic fatty liver disease, visceral fat accumulation, hepatic steatosis, NASH, TNF-α, estrogen, adiponectin, leptin, menopause, metabolic syndrome, BMI, obesity, fatty acid β-oxidation

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