Factors contributing to development of fatty liver and ketosis in lactating dairy cows

Abstract

Sixteen multiparous Holstein cows were assigned to one of three groups during d 14 to 42 postpartum: 1) control (fed ad libitum throughout), 2) 20% feed restriction, or 3) ad libitum plus dietary 1,3butanediol (5.5% of diet dry matter). From d 43 to 56 postpartum, cows assigned to both the feed-restricted and butanediol treatments received a combination of feed restriction and dietary butanediol. One cow quickly developed clinical ketosis but not fatty liver after only 4 d of feed restriction. No other cows subjected to the separate treatments of either feed restriction or dietary butanediol developed fatty liver or ketosis, nor did any cows subjected to the combination treatment from d 43 to 56 postpartum. Treatments decreased milk production. Concentrations of fihydroxybutyrate and insulin in plasma were increased by dietary 1,3butanediol. Feed restriction caused transient increases in concentrations of nonesterified fatty acids, acetate, and fi-hydroxybutyrate in plasma. Concentration of glycogen in liver was less in feed-restricted cows, whereas glycogen and total lipid in liver were greater from cows given dietary 1,3-butanediol separately. Gluconeogenic capacity of liver slices was not different among groups. Addition of L-carnitine to in vitro incubation media decreased conversion of propionate to glucose, whereas addition of either L-carnitine or 1,3-butanediol decreased oxidation of propionate to COg. Neither feed restriction nor dietary 1,3-butanediol as separate treatments during the early-postpartum period induced the fatty liver and ketosis seen in earlier experiments where the two treatments were given in combination starting at d 14 postpartum.