Antilipolytic and lipolytic effects of administering free or ruminally protected nicotinic acid to feed-restricted Holstein cows

2010 
Abstract The objectives were to determine effects of 12 hourly infusions of different quantities of nicotinic acid (NA) on plasma nonesterified fatty acid (NEFA; experiment 1) and whether longer (108h) continuous infusions of NA could induce sustained reductions of plasma NEFA (experiment 2) in nonlactating, nongestating Holstein cows that were feed restricted. Experiment 1 was a 5×5 Latin square with 6-d periods and 9 recovery days between each period. Each period consisted of 5 d of partial feed restriction to increase plasma NEFA concentration. Treatments were abomasal infusions of 0, 0.25, 0.5, 1, or 3mg of NA/h per kilogram of body weight (BW), infused as hourly boluses for 12h, starting 4 d after initiation of partial feed restriction. Plasma NEFA was decreased for the highest dose: from 448μEq/L to 138±75μEq/L at 1h after the first bolus of 3mg of NA/h per kilogram of BW. This initial reduction in plasma NEFA concentration was followed by an increase in concentration at 2, 3, and 4h relative to initiation of infusions. Plasma NEFA then decreased to 243μEq/L 6h after initiation of treatments and remained low until termination of infusions. A rebound in plasma NEFA concentration occurred at 3 and 4h after termination of infusion for cows that received 3mg of NA/h per kilogram of BW. Experiment 2 was a 5×5 Latin square with 7-d periods and 9 recovery days between each period. Each period consisted of 5 d of partial feed restriction to increase plasma NEFA concentration. Treatments were continuous abomasal infusion of 0, 0.5, 1, or 3mg of free NA/h per kilogram of BW for 4.5 d starting at feed restriction or 0.5mg of NA/h per kilogram of BW infused directly into the rumen in a form protected from microbial degradation. The ruminal administration of protected NA was initiated 2 d before abomasal infusions and initiation of feed restriction to establish steady postruminal delivery of NA by start of abomasal infusions. Plasma NEFA was approximately 70μEq/L before initiation of feed restriction and increased to 509, 587, 442, 850, and 108μEq/L at 4.5 d for cows that received 0, 0.5 (protected NA), 0.5 (free NA), 1, and 3mg of NA/h per kilogram of BW, respectively. An antilipolytic response was achieved with the highest abomasal dose, which maintained plasma NEFA concentration lower than the control group. An increase in plasma NEFA concentration was observed after termination of infusions for cows that received 1 and 3mg of NA/h per kilogram of BW. Plasma NEFA was 1,900μEq/L at 4h after termination of infusion for cows receiving 1mg of NA/h per kilogram of BW and 1,360μEq/L at 5h after termination of infusion for cows receiving 3mg of NA/h per kilogram of BW. In nongestating, nonlactating cows it is unlikely that a dose of NA exists that will reduce plasma NEFA concentration and prevent the rebound that occurs following termination of NA administration.
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