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

众所周知，奶牛脂肪肝与围产期疾病密切相关。因此，有必要阐明脂肪肝的发病机制，分析其发病机制，探讨脂肪肝的预防措施。本研究主要采用我们以前报道的禁食4天模型作为实验性诱导脂肪肝的方法。从生化、分子生物学和微观形态学等方面探讨了脂肪肝发生发展过程中的病理变化。部分研究还使用了乙硫氨酸诱导的脂肪肝奶牛样品。此外，我们还调查了一只偶然发现的患有局灶性脂肪肝（FFL）的奶牛。禁食4天后，血清游离脂肪酸浓度明显升高，诱发脂肪肝.脂肪肝发生发展过程中存在胰岛素抵抗.脂肪肝的微形态学观察可见基底膜增厚，星状细胞减少。免疫组化结果显示TNF α增高.随着脂肪肝的发展，门静脉血向肝细胞的总胆汁酸提取率降低.在脂肪肝中，极低密度脂蛋白向肝血中的分泌减少.乙硫氨酸诱发奶牛脂肪肝时载脂蛋白（apo）C-Ⅲ和apo B-100的下降模式明显不同。载脂蛋白C-Ⅲ浓度的变化与mRNA的变化相似。FFL病变局限于肝门静脉周围，内毒素可能是其发病原因之一。如上所述，获得了关于脂肪肝发病机制的有价值的发现。本实验拟详细研究基底膜、星状细胞与TNFα的关系。

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.