The objective was to examine the effects of insulin under euglycaemic conditions on liver long chain fatty acids (LCFA) metabolism with special focus on the aetiology of hepatic lipidosis in early lactation. A 4-day hyperinsulinaemic-euglycaemic clamp (clamp) was conducted on four dairy cows starting in weeks 4 and 17 postpartum. Insulin was infused continuously (1 mug/kg BW per h) and a 50 % glucose solution was infused to maintain euglycaemia. Liver biopsies were taken 6 days before, the last day of, and 5 days after the clamp, and blood samples were taken in the same period. In the liver tissue, the relative triglyceride content decreased (P < 0.01) and the glycogen content increased (P < 0.0001) in response to the clamp. Hepatic in vitro palmitate oxidation capacity was lowest during the clamp period and could be explained by a significant decrease in incomplete oxidation (ketogenesis) (P < 0.04) and a tendency to a decreased complete oxidation of palmitate (P < 0.10). Plasma non-esterified fatty acids concentration was decreased during the clamp in early lactation (P < 0.05) but there was no effect on the mid-lactation clamp. The present study shows that increased insulin under euglycaemic conditions seems to depress hepatic LCFA oxidation capacity. However, in terms of preventing hepatic lipidosis, the anti-lipolytic effect of insulin on adipose tissue, which results in decreased mobilization of and hence hepatic load with LCFA, appears more important.