Interactions of feed restriction and an exogenous source of ketone bodies (1,3-butanediol) in causing fatty liver and ketosis in dairy cows were studied. In experiment one, 16 cows were assigned to either control (fed ad libitum), feed restriction (fed 80% of ad libitum), or ad libitum plus 5.5% butanediol from day 14 through day 42 postpartum. From day 43 through d 56 postpartum, cows previously in either feed-restricted or dietary butanediol groups received the two treatments combined. Treatments decreased milk production. Concentrations in plasma of nonesterified fatty acids, acetate and [beta]-hydroxybutyrate were increased 200, 35, and 115% during the first week of feed restriction. Insulin and 3-hydroxybutyrate were increased 13 and 50% in cows given dietary butanediol. Liver glycogen was 25% greater in cows given butanediol and was 38% lower in feed-restricted cows. Hepatic content of total lipid tended to be greater in cows given butanediol. Conversion of propionate to glucose by liver slices decreased during treatment for all groups and was decreased 15% by addition of L-carnitine to incubation media. Combining feed restriction and dietary butanediol at d 43 postpartum decreased plasma glucose and increased 3-hydroxybutyrate. Neither feed restriction nor butanediol as separate treatments, nor combining the two at d 43 postpartum, caused development of fatty liver or ketosis;In experiment two, 13 cows were assigned to either control (fed ad libitum) or ketosis induction (fed 80% of ad libitum plus 7% 1,3-butanediol) from day 14 through day 42 postpartum. Six cows in the ketosis induction group developed subclinical ketosis, whereas the other cow quickly developed clinical ketosis. Milk production was decreased 20% and milk fat content increased 11% by subclinical ketosis. Energy balance reached a low of -6.6 Mcal/d during the first week of ketosis induction. In subclinically ketotic cows, concentrations of nonesterified fatty acids and [beta]-hydroxybutyrate were increased over twofold. Dextran sulfate-precipitable cholesterol and triglyceride in serum increased during the first week of ketosis induction. Liver triglyceride and glycogen increased 200% and 50% in subclinically ketotic cows. Oxidation of palmitate was greater in liver slices from ketosis-induction cows. Ratios of triglyceride to glycogen greater than 2.0 in liver during the early-postpartum period may indicate susceptibility to clinical ketosis
