cularization of the capsule; arterioles displace portal branches, which are extremely disordered and have no normal architecture.Arterio-portal shunt is also recognizable.
Estrogen effects were investigated on fatty liver induced by choline deficiency diet (CDD) in the rat. CDD-fed 83 male Wistar rats were divided into the following groups: (I) controls, fed with CDD alone (n=29); (II) rats received simultaneous injections of estradiol benzoate (EB) (n=30); (III) animals treated with EB from the third week of CDD exposure (n=24). EB was administered intramuscularly at a dose of 0.1 mg/100 g body weight three times weekly. All rats fed with CDD alone showed marked hepatocellular fatty changes with extremely narrowed sinusoids by two weeks of treatment, which led to hepatic fibrosis and liver cirrhosis with time. It is noteworthy, however, that these fibrotic changes were more conspicuous at the visceral surface of the liver than that of the diaphragmatic side. On the other hand, when simultaneously injected to rats with feeding of CDD, EB decreased and delayed the development of fatty change as well as of fibrosis in the liver. Furthermore, EB gave salutary effects on fully developed fatty liver of rats in group III, showing disappearance of fat droplets particularly in the periportal area accompanied by improved sinusoidal blood circulation. The results represent that disturbed sinusoidal blood flow due to an abundant fat accumulation in hepatocytes plays an important role in the progression of fatty liver to liver cirrhosis. In providing effective hepatic blood flow, EB exerts preventive and therapeutic effects on fatty liver induced by CDD.
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