title: Somatotropin increases protein balance independent of insulin's effects on protein metabolism in growing pigs.
abstract: Somatotropin (ST) administration enhances protein deposition and elicits profound metabolic responses, including hyperinsulinemia. To determine whether the anabolic effect of ST is due to hyperinsulinemia, pair-fed weight-matched growing swine were treated with porcine ST (150 microg x kg body wt(-1) x day(-1)) or diluent for 7 days (n = 6/group, approximately 20 kg). Then pancreatic glucose-amino acid clamps were performed after an overnight fast. The objective was to reproduce the insulin levels of 1) fasted control and ST pigs (basal insulin, 5 microU/ml), 2) fed control pigs (low insulin, 20 microU/ml), and 3) fed ST pigs (high insulin, 50 microU/ml). Amino acid and glucose disposal rates were determined from the infusion rates necessary to maintain preclamp blood levels of these substrates. Whole body nonoxidative leucine disposal (NOLD), leucine appearance (R(a)), and leucine oxidation were determined with primed, continuous infusions of [(13)C]leucine and [(14)C]bicarbonate. ST treatment was associated with higher NOLD and protein balance and lower leucine oxidation and amino acid and glucose disposals. Insulin lowered R(a) and increased leucine oxidation, protein balance, and amino acid and glucose disposals. These effects of insulin were suppressed by ST treatment; however, the protein balance remained higher in ST pigs. The results show that ST treatment inhibits insulin's effects on protein metabolism and indicate that the stimulation of protein deposition by ST treatment is not mediated by insulin. Comparison of the protein metabolic responses to ST treatment during the basal fasting period with those in the fully fed state from a previous study suggests that the mechanism by which ST treatment enhances protein deposition is influenced by feeding status.
authors.affiliation: United States Department of Agriculture, Agricultural Research Service (USDA/ARS) Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030, USA.
authors.forename: R C
authors.initials: RC
authors.lastname: Vann
authors.forename: H V
authors.initials: HV
authors.lastname: Nguyen
authors.forename: P J
authors.initials: PJ
authors.lastname: Reeds
authors.forename: N C
authors.initials: NC
authors.lastname: Steele
authors.forename: D R
authors.initials: DR
authors.lastname: Deaver
authors.forename: T A
authors.initials: TA
authors.lastname: Davis
mesh_terms: D000375:Aging / Q000378:metabolism*; D000818:Animals; D005947:Glucose / Q000378:metabolism; D013006:Growth Hormone / Q000494:pharmacology*; D006728:Hormones / Q000097:blood; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D007329:Insulin Antagonists / Q000494:pharmacology*; D007930:Leucine / Q000378:metabolism*; D010084:Oxidation-Reduction; D012016:Reference Values; D013552:Swine
chemical_list: D006728:Hormones; D007004:Hypoglycemic Agents; D007328:Insulin; D007329:Insulin Antagonists; D013006:Growth Hormone; D007930:Leucine; D005947:Glucose