4.7 Article

Effects of intraruminal infusion of sodium, potassium, and ammonium on hypophagia from propionate in lactating dairy cows

Journal

JOURNAL OF DAIRY SCIENCE
Volume 86, Issue 4, Pages 1398-1404

Publisher

AMER DAIRY SCIENCE ASSOC
DOI: 10.3168/jds.S0022-0302(03)73723-0

Keywords

propionate infusion; ammonium; urea synthesis; feeding behavior

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The objective of this experiment was to evaluate effects of salt type on hypophagic effects of intraruminal infusion of propionate in lactating dairy cows. Our working hypothesis is that oxidative metabolism of propionate causes satiety by increasing hepatic ATP concentration and decreasing the discharge rate of the hepatic vagus. We hypothesized that hypophagic effects of propionate are reduced by ammonium and potassium. We speculated that ammonium infusion lowers hepatic ATP concentration because ATP is used for urea synthesis and potassium increases the discharge rate of the hepatic vagus. Eight ruminally cannulated Holstein cows in midlactation were used in a duplicated 4 x 4 Latin square design experiment. Treatments were intraruminal infusion of propionic acid, ammonium propionate, sodium propionate, and potassium propionate. Treatment solutions were 0.93 M for propionate and 0.67 M for salts among the treatments except for propionic acid. Treatment solutions were infused over 14 h starting 2 h before feeding at 17.9 ml/min, which is equivalent to 16.7 and 11.9 mmol/min for propionate and salts, respectively. Infusion of ammonium propionate decreased dry matter intake compared with sodium propionate and potassium propionate (P < 0.04; 11.0 vs. 14.0 and 13.9 kg/12 h) by decreasing meal frequency without affecting meal size, indicating that ammonium delayed the sense of hunger. No difference in DMI and feeding behavior was observed between infusion of sodium and potassium propionate. Contrary to the hypothesis, ammonium infusion did not reduce hypophagic effects of propionate, possibly because the urea cycle indirectly stimulated oxidative metabolism in the liver by generating oxidizable carbon from amino acid catabolism.

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