Murondoti Absolom, Jorritsma Ruurd, Beynen Anton C, Wensing Theo, Geelen Math J H
Department of Nutrition, Graduate School of Animal Health, Faculty of Veterinary Medicine, Utrecht University, PO Box 80.152, 3508 TD Utrecht, The Netherlands.
J Dairy Res. 2004 May;71(2):129-34. doi: 10.1017/s0022029904000020.
The objective was to measure the activities of all the enzymes essential for hepatic gluconeogenesis in dairy cows with induced fatty liver. We aimed to induce severe fatty liver in ten experimental cows by overfeeding them during the dry period while seven control cows were maintained on a restricted diet. To induce a marked negative energy balance, the experimental cows were deprived of feed for 8 h immediately after parturition. In addition, the experimental cows were given a restricted amount of diet during the first 5 d of lactation. Liver samples were collected 1 week before and 1, 2 and 4 weeks after parturition. Before parturition, liver triacylglycerol concentrations did not differ between the two groups. After parturition, the experimental cows developed marked fatty liver as indicated by a higher level of triacylglycerols in the liver compared with the control cows. Before parturition, all gluconeogenic enzymes in the liver were lower in experimental cows than in control cows. Phosphoenolpyruvate carboxykinase, pyruvate carboxylase and propionyl-CoA carboxylase were significantly lower and fructose 1,6-bisphosphatase and glucose 6-phosphatase tended to be lower in the experimental cows. The activities of two crucial enzymes for gluconeogenesis in ruminants, i.e., phosphoenolpyruvate carboxykinase and propionyl-CoA carboxylase, remained low throughout the sampling period post partum. Activities of pyruvate carboxylase and glucose 6-phosphatase in the experimental cows post partum were upgraded to values similar to those of the control cows. The results showed that the capacity for hepatic gluconeogenesis before parturition was lower in cows with induced fatty liver than in control cows. After parturition, the low activities of crucial gluconeogenic enzymes indicated insufficient production of glucose. It is suggested that the low gluconeogenic capacity leads successively to low blood glucose concentrations, low insulin levels and high rates of mobilization of fatty acid, causing severe hepatic lipidosis.
目的是测定诱导性脂肪肝奶牛肝脏中糖异生所需的所有酶的活性。我们旨在通过在干奶期过度饲喂十头实验奶牛来诱导严重脂肪肝，而七头对照奶牛维持限制饮食。为诱导明显的负能量平衡，实验奶牛在分娩后立即禁食8小时。此外，实验奶牛在泌乳的前5天给予限量饮食。在分娩前1周以及分娩后1、2和4周采集肝脏样本。分娩前，两组肝脏三酰甘油浓度无差异。分娩后，实验奶牛出现明显脂肪肝，其肝脏中三酰甘油水平高于对照奶牛。分娩前，实验奶牛肝脏中所有糖异生酶均低于对照奶牛。磷酸烯醇式丙酮酸羧激酶、丙酮酸羧化酶和丙酰辅酶A羧化酶显著更低，实验奶牛中果糖1,6-二磷酸酶和葡萄糖6-磷酸酶也有降低趋势。反刍动物糖异生的两种关键酶，即磷酸烯醇式丙酮酸羧激酶和丙酰辅酶A羧化酶，在产后整个采样期活性一直较低。实验奶牛产后丙酮酸羧化酶和葡萄糖6-磷酸酶活性提升至与对照奶牛相似的值。结果表明，诱导性脂肪肝奶牛分娩前肝脏糖异生能力低于对照奶牛。分娩后，关键糖异生酶活性低表明葡萄糖生成不足。提示糖异生能力低会相继导致血糖浓度低、胰岛素水平低和脂肪酸动员率高，从而引起严重的肝脏脂质osis。
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