A BASIC STUDY ON THE MECHANISM OF FATTY LIVER OCCURRENCE IN DAIRY CATTLE

众所周知，奶牛的脂肪肝与围产期疾病密切相关。因此，阐明脂肪肝的发病机制，分析其发病机制，对探讨脂肪肝的防治措施具有重要意义。本研究主要采用我们以前报道的4天禁食模型作为实验性脂肪肝的诱导方法。从生化、分子生物学和微形态三个方面对脂肪肝发生发展过程中的病理变化进行了详细的阐述。乙硫氨酸诱导的脂肪肝奶牛的样本也被用于部分研究。此外，我们偶然遇到的一头患有局灶性脂肪肝(FFL)的奶牛也被调查了。结果：1.禁食4天后，大鼠血清游离脂肪酸浓度明显升高，并诱发脂肪肝。脂肪肝的发生发展过程中存在胰岛素抵抗。在脂肪肝的微形态分析中，可见基底膜增厚，星状细胞减少。免疫组织学上也证实了肿瘤坏死因子α升高。随着脂肪肝的发展，总胆汁酸从门静脉血到肝细胞的萃取率降低。脂肪肝中极低密度脂蛋白对肝脏血液的分泌减少。在乙硫氨酸诱导的奶牛脂肪肝模型中，载脂蛋白C-III的下降模式与载脂蛋白B-100的下降模式明显不同。载脂蛋白C-III的浓度变化与m-RNA的变化相似。FFL病变局限于肝门静脉周围，内毒素可能是其原因之一。如上所述，关于脂肪肝的发病机制得到了有价值的发现。我们计划对基底膜、星形细胞和肿瘤坏死因子α之间的关系进行详细的研究。

The fatty liver in dairy cattle is known to be closely linked to periparturient diseases. Therefore, it is essential to elucidate the mechanism in the induction of fatty liver together with analyzing the patho genesis in order to investigate the prophylaxis of the diseases. In this study, 4-days-fasting model reported previously by us was mainly used as a experimental induction of fatty liver. The changes of pathogenesis in the development of fatty liver were scrutinized biochemically, molecularbiologically and micromorphologically. The samples from cow with ethionine-induced fatty liver were also utilized in a part of study. Besides, a cow with focal fatty liver (FFL) we came across by chance was also investigated.1. By fasting for 4 days, serum concentration of free fatty acid was markedly increased and fatty liver was induced.2. Insulin resistance was observed in the development of fatty liver.3. In micromorphological analysis of fatty liver, increased thickness of basal lamina and decreased stellate cell was observed.. Increased TNF a were also admitted immunohistologically.4. The extraction rate of total bile acid from portal blood to hepatic cell was reduced with the development of fatty liver.5. Decreased secretion of very low density lipoprotein to hepatic blood was shown in the fatty liver.6. The decreased pattern of apolipoprotein (apo) C-III was distinctly different from that of apo B-100 in cow with ethionine-induced fatty liver. The change of apo C-III concentration was similar to that of the m-RNA.7. The lesion of FFL was localized around hepatic portal vein Endotoxin may be one of causes. As stated above, valuable findings regarding to the pathogenesis of fatty liver were obtained. We are planning to investigate the relation among basal lamina, stellate cell and TNFα in detail.