Dietary components impact metabolism early in life. Some of the diet-induced effects are long lasting, and can lead to various adult-based diseases. In the current studies, we examined the short term effects of dietary cholesterol on neonatal hepatic sterol metabolism, and the long term effects that those early life diets had on sterol metabolism in adulthood. Neonatal hamsters began consuming solid food as a supplement to milk by 5 days of age; diets contained 0 or 2% added cholesterol (wt/wt). By 10 days of age, plasma and liver cholesterol concentrations were 3.2- and 2.5-fold greater, respectively, in the neonates fed cholesterol. Hepatic sterol synthesis rates were suppressed 65% in cholesterol-fed neonates as compared to control neonates. By 20 days of age, plasma and liver cholesterol concentrations were still greater and sterol synthesis rates were now suppressed maximally in neonates fed cholesterol as compared to control neonates. Expression level of an apoB-containing lipoprotein receptor (LDL receptor-related protein; LRP) was greater and the mature form of the sterol regulatory element binding protein-2 (SREBP-2) was similar in livers of 20 day old control neonates as compared to control neonates at 10 days of age. To test if the change in sterol balance in the neonatal period had a lasting effect upon hepatic sterol metabolism, all animals were weaned onto a low cholesterol diet. At 70 days of age, hepatic sterol synthesis rates, plasma lipoprotein and liver cholesterol concentrations, and bile acid pool sizes and compositions were measured. Sterol balance in the adults was similar between animals fed either diet early in life as demonstrated by a lack of difference in any parameter measured. Thus, even though dietary cholesterol suppressed hepatic sterol synthesis rates dramatically in the neonatal hamster, the change has little impact upon sterol balance later in life.