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1 Nutritional Physiology Group, Department of Animal Science, Iowa State University, Ames 50011
Eighteen cows were assigned in equal numbers to three groups: control, ketosis induction by using feed restriction plus dietary 1,3-butanediol to provide ketone bodies, and glucose treatment with 484 g/d of glucose infused intraduodenally starting 7 d after beginning ketosis induction. Ketosis induction, begun at d 15 postpartum, caused ketonemia and gradual development of clinical ketosis by d 40 to 45. None of the cows in the control or glucose-treated groups became ketotic. Concentrations of NEFA in plasma of cows that became ketotic increased 3.0-, 2.6-, and 1.9-fold at 2 wk before, 2 wk before, and at ketosis, respectively, but increased nonsignificantly for glucose-treated cows. Concurrently, ß-hydroxybutyrate increased 3.5-, 5.8- and 8.4-fold for cows that became ketotic but 1.6-fold or less for glucose-treated cows. Plasma acetate increased dramatically 2 wk before ketosis. Liver glycogen content decreased to nearly 0 by 2 wk before ketosis occurred, but it increased to prepartal values in glucose-treated cows. Liver triglycerides averaged 2.0% of wet weight at d 5 for all cows but increased to 8 to 10% for about 2 wk before ketosis occurred. Microscopy of liver samples demonstrated progressive accumulation of lipid globules, which began in hepatocytes near the central vein and progressed toward the portal triad. Visible lipid content reached a peak 2 wk before ketosis. Hepatic in vitro gluconeogenic capacity decreased significantly for ketosis induction protocol cows when clinical ketosis was detected. Results indicate that experimental ketosis was preceded by metabolic abnormalities up to 2 wk before clinical ketosis occurred. The key events for onset of clinical ketosis, however, were not elucidated.
Key Words: ketosis • fatty liver • dairy cows
Submitted on December 26, 1990
Accepted on June 21, 1991
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