title: [Growth hormone insensitivity of rats under the endotoxemic condition].
abstract: OBJECTIVE
  To investigate the mechanism of growth hormone insensitivity of rats under the endotoxemic condition.
  
  
  METHODS
  Sprague Dawley rats (n = 180) were injected endotoxin, TNF-alpha, and IL-6 respectively. Part of endotoxin injected rats were treated with exogenous somatotropin simultaneously, and all rats were killed at different time points. Liver expression of IGF I, GHR and SOCS-3 mRNA was detected by RT-PCR, the levels of growth hormone (GH) were measured by radioimmunoassay, and the levels of TNF-alpha and IL-6 were detected by ELISA.
  
  
  RESULTS
  Serum GH levels showed no significant change after endotoxin injection; however, liver IGF I and GHR mRNA expressions were obviously down-regulated in endotoxemic rats, with the lowest decrease of 53% and 89% respectively. Although SOCS-3 mRNA was weakly expressed in control rats, it was strongly up-regulated in endotoxemic rats and the marked increase was 7.84 folds. The higher LPS dosage induced marked GHR mRNA down-regulation and marked SOCS-3 mRNA up-regulation. Exogenous GH made IGFI mRNA expression increase 25% in the control rats, but it did fail to prevent the decline in IGFI mRNA expression in endotoxemic rats. Endotoxin stimulated the production of TNF-alpha and IL-6, and the elevated IL-6 levels showed a positive correlation with increased SOCS-3 mRNA expression. Liver GHR mRNA expression was obviously down-regulated after TNF-alpha i.v. injection, but for IL-6, it mainly up-regulated the liver SOCS-3 mRNA expression.
  
  
  CONCLUSIONS
  The growth hormone insensitivity could be induced by LPS injection, which might be associated with down-regulated GHR mRNA expression and up-regulated SOCS-3 mRNA expression. The in vivo biological activities of LPS may be partially mediated by TNF-alpha and IL-6 at different aspects.
authors.affiliation: Institute of General Surgery, Jinling Hospital, Medical College of Nanjing University, Nanjing 210001, China. wpmd@Yahoo.com.cn
authors.forename: Ping
authors.initials: P
authors.lastname: Wang
authors.forename: Ning
authors.initials: N
authors.lastname: Li
authors.forename: Jieshou
authors.initials: J
authors.lastname: Li
authors.forename: Weiqin
authors.initials: W
authors.lastname: Li
mesh_terms: D000818:Animals; D015536:Down-Regulation; D013006:Growth Hormone / Q000378:metabolism* / Q000494:pharmacology; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000494:pharmacology / Q000502:physiology; D008070:Lipopolysaccharides / Q000633:toxicity*; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011986:Receptors, Somatotropin / Q000235:genetics; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology / Q000502:physiology
chemical_list: D015850:Interleukin-6; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D011986:Receptors, Somatotropin; D050826:Suppressor of Cytokine Signaling Proteins; D014409:Tumor Necrosis Factor-alpha; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone