Two experiments were conducted to test the following two hypotheses: 1)
fatty liver could hamper hepatic conversion of
ammonia to
urea and increase circulating
ammonia or Gln% [Gln% = Gln x 100/(Gln + Glu)] in cows around parturition; 2) decreased ureagenesis might cause
alkalosis and in turn reduce blood Ca. In the first experiment, 14 Holstein cows were monitored from 27 d prepartum to 35 d postpartum. There was a rise in circulating
ammonia and Gln% at calving, suggesting an increase in
ammonia passing to and through the liver. Stepwise regression analysis revealed the following relationship for plasma samples at 22 h and liver
triglyceride at 2 d postpartum:
ammonia (microM) = 32.1+/-0.89
triglyceride (% DM), Gln% = 71.2 + 0.23
triglyceride (% DM) + 1.31
urea (mM). The positive correlation between liver
triglyceride and plasma
ammonia and Gln% suggests that hepatic
triglyceride accumulation might inhibit ureagenesis, thereby increasing
ammonia concentration at the perivenous hepatocytes where Gln synthesis occurs and increasing
ammonia concentration in blood leaving the liver. In the second experiment, 28 rats were used to determine whether hepatic
triglyceride accumulation, induced by
choline deficiency, affects urinary
ammonia N and blood pH homeostasis. There was a trend for a positive correlation between urinary
ammonia N and liver
triglyceride. No correlation between liver
triglyceride and blood pH,
bicarbonate, pCO2 or plasma Ca was found. In conclusion, hepatic
triglyceride accumulation may inhibit ureagenesis and result in increased circulating
ammonia, Gln% and urinary
ammonia N in vivo. Hepatic
triglyceride accumulation did not affect blood pH homeostasis.