Böhm S A, Wolf M, Kreymann G, Hölscher A H
Klinik und Poliklinik für Visceral- und Gefässchirurgie, Universität zu Köln.
Langenbecks Arch Chir Suppl Kongressbd. 1998;115(Suppl I):185-8.
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.
危重病与多种激素系统改变所引起的分解代谢有关。尽管生长激素（GH）水平升高或正常，但在危重病中仍观察到胰岛素样生长因子I（IGF-I）水平较低。这种明显的GH抵抗机制尚未阐明。由于促炎细胞因子介导了危重病中的许多急性反应，我们评估了白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）对培养的大鼠肝细胞中生长激素受体（GHR）-mRNA的影响。细胞因子刺激后GHR-mRNA浓度降低表明，在严重疾病初期IGF-I水平较低，可能至少部分是促炎细胞因子抑制GHR合成的原因。
