[Pro-inflammatory cytokines IL-1 beta and TNF-alpha reduce growth hormone receptor mRNA concentration in cultivated rat hepatocytes after stimulation with growth hormone].
Critical illness is associated with catabolism caused by the alteration of several hormonal systems. Low levels of insulin-like growth factor I (IGF-I) in critical illness are observed despite increased or normal levels of growth hormone (GH). The mechanisms for this apparent GH resistance have not been elucidated. Since proinflammatory cytokines mediate many of the acute responses in critical illness, we evaluated the effects of IL-1 beta and TNF-alpha on growth hormone receptor-(GHR-)mRNA in cultured rat hepatocytes. Diminished GHR-mRNA concentrations in response to cytokine stimulation indicate that low IGF-I levels in the beginning of severe illness, may at least be partially a cause of GHR synthesis suppression by proinflammatory cytokines.
D000818:Animals; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D015870:Gene Expression / Q000187:drug effects; D013006:Growth Hormone / Q000494:pharmacology*; D066298:In Vitro Techniques; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007375:Interleukin-1 / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D012333:RNA, Messenger / Q000187:drug effects* / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D011986:Receptors, Somatotropin / Q000037:antagonists & inhibitors / Q000235:genetics*; D013268:Stimulation, Chemical; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D007375:Interleukin-1; D012333:RNA, Messenger; D011986:Receptors, Somatotropin; D014409:Tumor Necrosis Factor-alpha; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone