Somatotropin-induced amino acid conservation in pigs involves differential regulation of liver and gut urea cycle enzyme activity.
Somatotropin (ST) treatment promotes animal growth and allows for the conservation of amino acids by increasing nitrogen retention and reducing ureagenesis and amino acid oxidation. To determine whether the improvement in amino acid conservation with ST treatment involves regulation of urea cycle enzyme activities in both liver and intestine, growing swine were treated with either ST (150 microg x kg(-1) x d(-1)) or saline for 7 d. Fully fed pigs (n = 20) were infused intravenously for 2 h with NaH(13)CO(3) followed by a 4-h intraduodenal infusion of [1-(13)C]phenylalanine. Arterial and portal venous blood and breath samples were obtained at baseline and steady-state conditions for measurement of amino acid and blood urea nitrogen (BUN) concentrations and whole-body phenylalanine oxidation. Urea cycle enzyme activities were determined in liver and jejunum. ST decreased BUN (-46%), arterial (-34%) and portal venous (-43%) amino acid concentrations and whole-body phenylalanine oxidation (-30%). The activities of carbamoylphosphate synthase-I (-45%), argininosuccinate synthase (-38%), argininosuccinate lyase (-23%), arginase (-27%), and glutaminase (-18%), but not of ornithine carbamoyltransferase, ornithine aminotransferase, or glutamate dehydrogenase were reduced in liver of ST-treated pigs. ST slightly increased intestinal activity of glutaminase (+9%) but did not affect that of any other enzymes. ST decreased hepatic, but increased jejunal, N-acetylglutamate (an essential allosteric activator of carbamoylphosphate synthase-I; -26% and +32%, respectively) and carbamoylphosphate (a substrate for ornithine carbamoyltransferase; -20% and +28%, respectively) content. These results demonstrate that the reduced amino acid catabolism with ST treatment in growing pigs involves a reduction in hepatic urea cycle enzyme activities. The effect of ST treatment on porcine urea cycle enzymes is tissue-specific and is associated with a reduction in substrate availability for hepatic ureagenesis.
Bush
Jill A
JA
U.S. Department of Agriculture/Agricultural Research Service Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA.
Wu
Guoyao
G
Suryawan
Agus
A
Nguyen
Hanh V
HV
Davis
Teresa A
TA
D000596:Amino Acids / Q000097:blood* / Q000378:metabolism; D000641:Ammonia / Q000097:blood; D000818:Animals; D001639:Bicarbonates / Q000097:blood; D001806:Blood Urea Nitrogen; D001835:Body Weight / Q000187:drug effects; D001944:Breath Tests; D002221:Carbamyl Phosphate / Q000378:metabolism; D002247:Carbon Isotopes; D005260:Female; D005971:Glutamates / Q000378:metabolism; D013006:Growth Hormone / Q000494:pharmacology*; D007583:Jejunum / Q000201:enzymology*; D008099:Liver / Q000201:enzymology*; D009584:Nitrogen / Q000378:metabolism; D010084:Oxidation-Reduction; D010649:Phenylalanine / Q000378:metabolism; D011897:Random Allocation; D013379:Substrate Specificity; D013552:Swine / Q000097:blood / Q000254:growth & development*; D014508:Urea / Q000378:metabolism
D000596:Amino Acids; D001639:Bicarbonates; D002247:Carbon Isotopes; D005971:Glutamates; D010649:Phenylalanine; D002221:Carbamyl Phosphate; D000641:Ammonia; D014508:Urea; D013006:Growth Hormone; C016195:N-acetylglutamic acid; D009584:Nitrogen