Nakano M
Acta Pathol Jpn. 1986 Nov;36(11):1643-52. doi: 10.1111/j.1440-1827.1986.tb02228.x.
Examination of hepatic fibrosis induced by choline deficient diet showed the histogenesis of early fibrosis and septa formation. Male rats were fed a choline deficient diet. Groups of three were sacrificed after 1, 2, 3, 6, 8, 12, and 13 weeks. Control groups of three rats were sacrificed after 6, 8, and 12 weeks. All choline deficient rats showed initial steatosis around the portal tracts. The fat droplets were small at first and gave a microvesicular appearance. As they grew, they gathered around the terminal hepatic venule by the 3rd week. Then, reticular fibers developed around the hepatocytes in the centrolobular area and fibroses connected the terminal hepatic venules. The fat droplets became larger and made nodular masses around the portal tract. These compressed the fibroses to the periphery where they formed septa. After 12 weeks, regenerating nodules developed. Electron microscopy showed that fat storing cells helped cause pericellular fibrosis.
对胆碱缺乏饮食诱导的肝纤维化进行检查显示了早期纤维化的组织发生和间隔形成。雄性大鼠喂食胆碱缺乏饮食。每组三只大鼠在1、2、3、6、8、12和13周后处死。三只大鼠的对照组在6、8和12周后处死。所有胆碱缺乏的大鼠在门静脉周围均出现初始脂肪变性。脂肪滴起初很小,呈微泡状外观。随着它们的生长,到第3周时它们聚集在终末肝小静脉周围。然后,小叶中心区的肝细胞周围出现网状纤维,纤维化连接终末肝小静脉。脂肪滴变大,在门静脉周围形成结节状肿块。这些将纤维化挤压到外周,在那里形成间隔。12周后,出现再生结节。电子显微镜显示,贮脂细胞有助于引起细胞周围纤维化。