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1 Nutritional Physiology Group, Department of Animal Science, Iowa State University, Ames 50011
Previous research has shown that a combination of feed restriction and dietary 1,3-butanediol starting at 14 d post-partum resulted in fatty liver and ketosis. Sixteen multiparous Holstein cows were used to determine effects of feed restriction or 1,3-butanediol as separate treatments. Treatments during d 14 to 42 postpartum were 1) control (ad libitum intake), 2) 20% feed restriction, or 3) control plus dietary 1,3-butanediol (5.5% of DM). From d 43 to 56, cows assigned to treatments 2 and 3 received a combination of feed restriction and butanediol. One cow on treatment 2 developed ketosis, but not fatty liver, after only 4 d of feed restriction. No other cows developed fatty liver or ketosis. Both treatments decreased milk production compared with controls. Feed restriction increased the extent of negative energy balance and caused transient increases in concentrations of NEFA, acetate, and ß-hydroxybutyrate in plasma. Concentrations of ß-hydroxybutyrate and insulin in plasma were increased by butanediol, which is a potent ketone body precursor. Concentration of glycogen in liver was less in feed-restricted cows, whereas glycogen and total lipid were greater in cows given butanediol separately. Gluconeogenic capacity of liver slices was not different among groups. Addition of 1,3-butanediol to in vitro incubation media decreased oxidation of propionate to CO2. Neither feed restriction nor dietary 1,3-butanediol as separate treatments induced the fatty liver and ketosis observed in earlier experiments in which the two treatments were given together.
Key Words: fatty liver • ketosis • dairy cows
Submitted on December 26, 1990
Accepted on May 15, 1991
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