Liver Metabolism and the Transition Cow

The periparturient period of the lactation cycle in dairy cattle is characterized by dramatic changes in nutrient demand that necessitate exquisite coordination of metabolism to meet requirements for energy, glucose, and amino acids by the mammary gland following calving. To meet their energy requirements during the first weeks of lactation, dairy cows mobilize large quantities of fatty acids from adipose tissue, resulting in increased circulating concentrations of nonesterified fatty acids (NEFA). The NEFA are used by peripheral tissues as an energy source and incorporated into milk fat, but also are extracted by the liver from the circulation in proportion to their supply (1). The NEFA extracted by the liver are oxidized or esterified into triglycerides and either exported in very low density lipoproteins (VLDL) or accumulated in liver tissue (2). The capacity of ruminant liver to oxidize fatty acids or export triglycerides in VLDL is limited (2); therefore, if mobilization of fatty acids from adipose tissue is excessive, the capacity of the liver to either export or oxidize fatty acids is exceeded and fatty acids accumulate as triglycerides in liver tissue. Furthermore, a consequence of partial oxidation of fatty acids is the formation of ketone bodies and, potentially, ketosis. Estimates of the prevalence of moderate or severe fatty liver in cows vary widely [35% (3) to 66% (4)], yet it is likely that all cows accumulate at least some triglycerides in liver during the first few days after calving. More uncertain is the threshold of liver triglyceride accumulation that results in morbidity to the cow. Recent evidence indicates that triglyceride accumulation impairs ureagenic capacity of liver (5), which probably impairs gluconeogenic capacity (6). The net result of this metabolic impairment seems to be decreased feed intake and milk production (7,8), increased incidence of disease (3), and subsequently decreased reproductive performance (4,9,10,11).