NUTRITIONAL REGULATION OF INSULIN-LIKE GROWTH-FACTOR-I
NUTRITIONAL REGULATION OF INSULIN-LIKE GROWTH-FACTOR-I
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DOI：
10.1016/0026-0495(95)90221-x
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发表时间：
1995-10-01
影响因子：
9.8
通讯作者：
THISSEN, JP
中科院分区：
文献类型：
--
作者：
KETELSLEGERS, JM;MAITER, D;THISSEN, JP
几条证据表明，在人类中，胰岛素样生长因子-I（IGF-I）是营养调节的。维持IGF-I需要能量和蛋白质。血清IGF I的测量构成了监测急性病患者对营养干预的反应的敏感手段。血清IGF-I也可作为营养状况评价的指标。我们的研究结果和其他人在动物模型中的研究结果表明，营养素在多个水平上影响IGF-I及其结合蛋白（IGFBPs）的合成和作用。在禁食时，肝脏生长激素（GH）结合减少，为IGF-I减少提供了一种解释。在蛋白质限制中，GH受体得以维持，但有证据表明存在受体后缺陷。后者由翻译前和翻译缺陷引起。肝细胞的氨基酸可用性对IGF-I基因表达至关重要。蛋白质营养不良不仅降低了IGF-I的产生率，而且还增加了其血清清除和降解。最后，有证据表明，在蛋白质限制的大鼠中，选择性器官对IGF-I的促生长作用具有抵抗力。版权所有（C）1995由W.B.桑德斯公司
Several lines of evidence indicate that in the human, insulin like growth factor-I (IGF-I) is nutritionally regulated. Both energy and protein availability are required for maintenance of IGF-I. Measurements of serum IGF I constitute a sensitive means for monitoring the response of acutely ill patients to nutritional intervention. Serum IGF-I may also serve as a marker for evaluation of nutritional status. Our findings and those of others in animal models suggest that nutrients influence synthesis and action of IGF-I and its binding proteins (IGFBPs) at multiple levels. In fasting, liver growth hormone (GH) binding is decreased, providing one explanation for decreased IGF-I. In protein restriction, GH receptors are maintained, but there is evidence for a postreceptor defects. The latter results from pretranslational and translational defects. Amino acid availability to the hepatocytes is essential for IGF-I gene expression. Protein malnutrition not only decreases IGF-I production rate, but also enhances its serum clearance and degradation. Finally, there is evidence for selective organ resistance to the growth-promoting effects of IGF-I in protein restricted rats. Copyright (C) 1995 by W.B. Saunders Company.