title: Effect of growth hormone or chromium picolinate on swine metabolism and inflammatory cytokine production after endotoxin challenge exposure.
abstract: OBJECTIVE
  To determine whether recombinant porcine somatotropin (PST) or chromium picolinate (CrP) affected cytokine production and metabolism in swine after endotoxin challenge exposure.
  
  
  METHODS
  20 Poland China X Landrace pigs, 5/group.
  
  
  METHODS
  Pigs were given CrP-supplemented feed at body weight of 20 kg; PST treatment began at 60 kg, and both treatments continued through body weight of 90 kg. At 90 kg, pigs were challenge exposed with 20 micrograms of lipopolysaccharide (LPS)/kg of body weight. Blood samples were obtained at various times through 24 hours after LPS challenge exposure.
  
  
  RESULTS
  In all pigs not given PST, glucose concentration decreased 2 to 4 hours after LPS. In PST-treated pigs, blood glucose concentration was decreased at 6 to 8 hours after LPS. Plasma insulin concentration paralleled changes in glucose concentration. Nonesterified fatty acid concentration was high 2 to 24 hours after LPS in pigs not given PST and at 6 to 24 h in PST-treated pigs. Plasma urea nitrogen concentration was high at 6 to 24 hours after LPS in pigs not given PST. The urea nitrogen values in PST-treated pigs were lower at all times. Serum aspartate transaminase activity was high 6 to 24 hours after LPS in pigs not given PST, whereas PST treatment prevented the increase in this enzyme activity. In untreated (PST) pigs, plasma bilirubin (total and direct) concentrations were high 4 to 8 hours after LPS and returned to normal at 24 hours. The PST- and CrP-treated pigs maintained normal plasma bilirubin concentrations. Interleukin 6 activity was unaffected by CrP and PST treatments. Treatment with CrP and PST decreased the tumor necrosis factor alpha response to LPS, compared with that in control pigs.
  
  
  CONCLUSIONS
  PST, and to a lesser extent CrP, provide protection against the adverse metabolic effects of LPS-induced septic shock.
authors.affiliation: Animal Biology Branch, USFDA/Center for Veterinary Medicine, Laurel, MD 20708, USA.
authors.forename: M J
authors.initials: MJ
authors.lastname: Myers
authors.forename: D E
authors.initials: DE
authors.lastname: Farrell
authors.forename: C M
authors.initials: CM
authors.lastname: Evock-Clover
authors.forename: M W
authors.initials: MW
authors.lastname: McDonald
authors.forename: N C
authors.initials: NC
authors.lastname: Steele
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D001663:Bilirubin / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D001806:Blood Urea Nitrogen; D001835:Body Weight; D016207:Cytokines / Q000096:biosynthesis*; D004926:Escherichia coli / Q000378:metabolism; D004927:Escherichia coli Infections / Q000097:blood / Q000378:metabolism / Q000662:veterinary; D005230:Fatty Acids, Nonesterified / Q000097:blood; D013006:Growth Hormone / Q000494:pharmacology*; D007328:Insulin / Q000097:blood; D015850:Interleukin-6 / Q000032:analysis / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000378:metabolism / Q000633:toxicity*; D010848:Picolinic Acids / Q000494:pharmacology*; D011994:Recombinant Proteins / Q000494:pharmacology; D013552:Swine / Q000097:blood / Q000254:growth & development / Q000378:metabolism*; D013553:Swine Diseases / Q000097:blood / Q000378:metabolism; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000096:biosynthesis
chemical_list: D001786:Blood Glucose; D016207:Cytokines; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D015850:Interleukin-6; D008070:Lipopolysaccharides; D010848:Picolinic Acids; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D013006:Growth Hormone; D001219:Aspartate Aminotransferases; C030614:picolinic acid; D001663:Bilirubin