Interleukin-1β suppresses growth hormone-induced acid-labile subunit mRNA levels and secretion in primary hepatocytes
Interleukin-1β suppresses growth hormone-induced acid-labile subunit mRNA levels and secretion in primary hepatocytes
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DOI：
10.1006/bbrc.1998.8089
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发表时间：
1998-02-04
影响因子：
3.1
通讯作者：
Delhanty, PJD
中科院分区：
文献类型：
--
作者：
Delhanty, PJD
细胞因子被认为介导由感染和创伤诱导的分解代谢状态。最近的证据表明，细胞因子白细胞介素-1 β（IL-1 β）直接抑制合成代谢胰岛素样生长因子（IGF）-I：生长激素（GH）轴。循环IGF的生物活性受肝细胞衍生的140-kDa IGF结合蛋白（IGFBP）复合物的GH依赖性酸不稳定亚基（ALS）调节。ALS通过将胰岛素样生长因子与IGFBP-3隔离在三元复合物中来缓冲胰岛素样生长因子的生长和代谢作用。为了确定IL-1 β是否对肝ALS产生有直接影响，我们研究了其对ALS mRNA水平和在OH诱导和基础条件下肝细胞分泌的影响。在GH（30 ng/mL）存在下，0.3-3 ng/mL rhIL-1 β可诱导ALS mRNA水平和分泌的半数最大降低（P < 0.05）。然而，在基础条件下，IL-1 β对ALS mRNA水平没有显著影响，仅轻微抑制分泌。我们的研究表明，IL-1 β调节ALS基因的表达和分泌的方式是依赖于，在某种程度上，与GH信号通路的相互作用。(C)北京：科学出版社.
Cytokines are thought to mediate the catabolic states induced by infection and trauma. Recent evidence suggests that the cytokine interleukin-1 beta (IL-1 beta) directly inhibits the anabolic insulin-like growth factor (IGF)-I:growth hormone (GH) axis. The biological activity of circulating IGF is regulated by the hepatocyte derived, GH-dependent acid-labile subunit (ALS) of the 140-kDa IGF binding protein (IGFBP) complex. ALS buffers the growth and metabolic effects of the insulin-like growth factors by sequestering them in a ternary complex with IGFBP-3. To determine whether IL-1 beta has a direct effect on hepatic ALS production, we have examined its effect on ALS mRNA levels and secretion in hepatocytes under OH-induced and basal conditions. In the presence of GH (30 ng/mL) half-maximal reduction of ALS mRNA levels and secretion was induced by between 0.3-3 ng/mL rhIL-1 beta (P < 0.05). However, under basal conditions IL-1 beta had no significant effect on ALS mRNA levels, and only a slight suppression of secretion. Our study suggests that IL-1 beta regulates ALS gene expression and secretion in a way that is dependent, in part, on interaction with the GH signalling pathway. (C) 1998 Academic Press.