Effects of induced parturition and estradiol on feed intake, liver triglyceride concentration, and plasma metabolites of transition dairy cows.
The effect of induced parturition and estradiol on feed intake, liver triglyceride, plasma metabolites, and milk yield was evaluated in fifty-six Holstein cows and heifers. Cows were assigned to treatments on d 260 of gestation and were on trial until d 10 postpartum for measurement of dry matter intake (DMI), plasma metabolites, and liver triglyceride and until d 31 postpartum to measure milk yield. Fourteen animals per group (9 cows and 5 heifers) received either a placebo, 1 mg of fenprostalene, 50 mg of estradiol-17 beta benzoate, or both on d 276 of gestation. Cows that received fenprostalene consumed more dry matter (DM) for the last 8 d prepartum than did cows that did not receive fenprostalene (9.6 kg/d vs. 8.5 kg/d, respectively) but consumed less DM for the first 10 d postpartum (10.9 kg/d vs. 13.1 kg/d, respectively). Cows injected with estradiol-17 beta benzoate tended to consume less DM postpartum than did cows not injected with estradiol-17 beta benzoate (11.3 kg/d vs. 12.7 kg/d, respectively). There was no effect of treatment on milk yield; however, a fenprostalene by day interaction resulted from lower milk yield on d 3, 4, 5, 7, and 10 relative to calving in cows that received fenprostalene. Administration of fenprostalene resulted in a delay in the peak plasma nonesterified fatty acid (NEFA) concentration until 2 d after calving. Plasma glucose concentrations were greatest 1 d prior to calving for cows that received fenprostalene, whereas plasma glucose concentrations peaked on the day of calving for cows that did not receive fenprostalene. Liver triglyceride increased over time; however, there was no effect of treatment on liver triglyceride. Calving induction improved DMI for the last 8 d prepartum, but a concomitant decrease in liver triglyceride after calving did not result. Estradiol-17 beta benzoate had no effect on plasma metabolites or liver triglyceride, indicating that the physiological rise in estradiol prior to calving does not have a primary role in lipolysis or hepatic fatty acid metabolism in the dairy cow.
Bremmer
D R
DR
Department of Dairy Science, University of Wisconsin, Madison 53706, USA.
Christensen
J O
JO
Grummer
R R
RR
Rasmussen
F E
FE
Wiltbank
M C
MC
D000020:Abortifacient Agents, Nonsteroidal / Q000494:pharmacology*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002417:Cattle; D002149:Energy Intake; D004958:Estradiol / Q000494:pharmacology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005247:Feeding Behavior; D005260:Female; D007751:Labor, Induced / Q000662:veterinary*; D007774:Lactation / Q000187:drug effects; D016018:Least-Squares Analysis; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008892:Milk / Q000187:drug effects / Q000378:metabolism*; D049590:Postpartum Period / Q000502:physiology*; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D011461:Prostaglandins F, Synthetic / Q000494:pharmacology*; D013997:Time Factors; D014280:Triglycerides / Q000097:blood*
D000020:Abortifacient Agents, Nonsteroidal; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D011461:Prostaglandins F, Synthetic; D014280:Triglycerides; D004958:Estradiol; C039153:fenprostalene