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Etiology of lipid-related metabolic disorders in periparturient dairy cows.

Plasma NEFA concentrations increase prior to and at parturition, resulting in increased fatty acid uptake by the liver, fatty acid esterification, and triglyceride storage. Liver triglyceride concentration increases four- to fivefold between d 17 prior to calving and d 1 following calving. Increases in liver triglyceride following calving do not appear to be dramatic. Severity of fatty liver 1 d postpartum is correlated negatively with feed intake 1 d prepartum. Export of newly synthesized triglyceride as very low density lipoprotein occurs slowly in ruminants and is a major factor in the development of fatty liver. Nutritional strategies to minimize the elevation in plasma NEFA prior to calving results in lower liver triglyceride at calving. Fatty liver probably precedes clinical spontaneous ketosis. Liver triglyceride to glycogen ratio may be used to predict susceptibility of cows to ketosis. Consequently, strategies to reduce liver triglyceride at calving may decrease incidence of ketosis. Research to determine methods to reduce fatty acid delivery to the liver or to enhance hepatic export of very low density lipoprotein near calving is warranted. Identification of the cause for the slow rate of assembly and secretion of hepatic very low density lipoprotein in ruminants will be required to assess the feasibility of increasing export of very low density lipoprotein.