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Journal of Dairy Science Vol. 73 No. 6 1537-1543
© 1990 by American Dairy Science Association ®
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Estrogen Induction of Fatty Liver in Dairy Cattle

Ric R. Grummer 1, Sandra J. Bertics 1, David W. Lacount 1, Jane A. Snow 1, M. R. Dentine 1, and Ralph H. Stauffacher 1

1 Department of Dairy Science, University of Wisconsin, Madison 53706

Two trials were conducted to determine if estrogen contributes to development of fatty liver in dairy cattle. During trial 1, eight late lactation, nonpregnant cows were assigned to 0 or 15 mg estradiol-17ß benzoate/d treatment. Days 1 to 3 of the trial were for baseline measurements, and treatments were given from d 4 to 21; on d 20 and 21 animals were fasted. Short-term feed deprivation resulted in increased plasma FFA concentrations and rapid accumulation of triglyceride into liver tissue obtained by biopsy. During starvation, plasma FFA concentration and liver triglyceride content were lower for cows receiving the estradiol-17ß treatment relative to cows receiving control treatment. Very low density lipoprotein concentration in blood increased dramatically in three of four animals during estradiol-17ß administration. Because of the decrease in milk production during estradiol-17ß treatment, it was not known whether this represented a decrease in very low density lipoprotein clearance from blood or reflected a lipotropic response to estradiol-17ß. Therefore, a second trial was conducted employing nonlactating cows, and control and estradiol-17ß-treated animals were pair fed. The trial was 33 d with d 1 to 3 for baseline measurements, and treatments were administered from d 4 to 33. All animals were starved from d 19 to 23. Estradiol-17ß increased hepatic lipid and triglyceride accumulation and plasma very low density lipoprotein concentration during starvation. Plasma FFA concentration was also increased by estradiol-17ß during this time; therefore, a direct or indirect effect of estrogen on hepatic lipid metabolism could not be delineated.

Key Words: estrogen • fatty liver • lipotropic • response

Submitted on September 11, 1989
Accepted on December 28, 1989




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