Plasma NEFA concentrations increase prior to and at parturition, resul
ting in increased fatty acid uptake by the liver, fatty acid esterific
ation, and triglyceride storage. Liver triglyceride concentration incr
eases four- to fivefold between d 17 prior to calving and d 1 followin
g calving. Increases in liver triglyceride following calving do not ap
pear to be dramatic. Severity of fatty liver 1 d postpartum is correla
ted negatively with feed intake 1 d prepartum. Export of newly synthes
ized triglyceride as very low density lipoprotein occurs slowly in rum
inants and is a major factor in the development of fatty liver. Nutrit
ional strategies to minimize the elevation in plasma NEFA prior to cal
ving results in lower liver triglyceride at calving. Fatty liver proba
bly precedes clinical spontaneous' ketosis. Liver triglyceride to glyc
ogen ratio may be used to predict susceptibility of cows to ketosis. C
onsequently, strategies to reduce liver triglyceride at calving may de
crease incidence of ketosis. Research to determine methods to reduce f
atty acid delivery to the liver or to enhance hepatic export of very l
ow density lipoprotein near calving is warranted. Identification of th
e cause for the slow rate of assembly and secretion of hepatic very lo
w density lipoprotein in ruminants will be required to assess the feas
ibility of increasing export of very low density lipoprotein.