Nutritional regulation of the insulin-like growth factors.
Nutritional regulation of the insulin-like growth factors.
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DOI：
10.1210/edrv-15-1-80
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发表时间：
1994-02
影响因子：
20.3
通讯作者：
J. Thissen;J. Ketelslegers;L. Underwood
中科院分区：
文献类型：
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作者：
J. Thissen;J. Ketelslegers;L. Underwood
营养是循环IGF-I的主要调节剂之一。在人类中，血清IGF-I浓度显着降低能量和/或蛋白质剥夺。能量和蛋白质在调节血清IGF-I浓度方面都至关重要。事实上，禁食后，能量和蛋白质的最佳摄入对于快速恢复循环IGF-I是必要的。然而，我们认为，在成年人中，能量在这方面可能比蛋白质更重要。虽然最低的蛋白质摄入量能够在足够能量的情况下增加IGF-I，但存在一个阈值能量需求，低于该阈值，最佳蛋白质摄入量在禁食后不能提高IGF-I。当能量摄入严重减少时，饮食中的碳水化合物含量是IGF-I对GH反应性的主要决定因素。当蛋白质摄入量减少时，饮食中的必需氨基酸含量对于禁食后IGF-I的最佳恢复也至关重要。循环IGF-I对营养物质的敏感性、其浓度的昼夜稳定性及其相对较短的半衰期构成了其用作营养状况和营养恢复充分性的标志物的基础。对于这些适应症，IGF-I测量比其他营养相关血清蛋白（白蛋白，前白蛋白，转铁蛋白，视黄醇结合蛋白）的测量更敏感，更特异。已经开发了动物模型来研究负责IGF-I的营养调节的机制。毫无疑问，这涉及到许多机制（图12）。饮食限制时血清IGF-I的下降与饮食诱导的垂体GH分泌的改变无关。肝脏GH受体的作用取决于营养损伤的严重程度。在严重的饮食限制（禁食），显着减少的体细胞受体的数量支持的作用，受体缺陷循环IGF-I的下降。相反，在不太严重的形式的饮食限制（蛋白质限制），IGF-I的下降结果从受体后缺陷的GH行动在肝脏水平。营养缺乏通过减少IGF-I基因表达来减少肝脏IGF-I的产生。IGF-I基因表达的下降主要是由营养缺乏引起的，其次是营养诱导的激素变化（胰岛素和T3）。饮食限制还通过改变循环IGFBPs水平增加血清IGF-I的清除和降解。（400字处截断摘要）
Nutrition is one of the main regulators of circulating IGF-I. In humans, serum IGF-I concentrations are markedly lowered by energy and/or protein deprivation. Both energy and proteins are critical in the regulation of serum IGF-I concentrations. Indeed, after fasting, optimal intake of both energy and protein is necessary for the rapid restoration of circulating IGF-I. We believe, however, that in adult humans energy may be somewhat more important than protein in this regard. While the lowest protein intake is able to increase IGF-I in the presence of adequate energy, there is a threshold energy requirement below which optimal protein intake fails to raise IGF-I after fasting. When energy intake is severely reduced, the carbohydrate content of the diet is a major determinant of responsiveness of IGF-I to GH. The essential amino acid content of the diet is also critical for the optimal restoration of IGF-I after fasting, when protein intake is reduced. The exquisite sensitivity of circulating IGF-I to nutrients, the nycthemeral stability of its concentrations and its relative short half-life constitute the basis for its use as a marker of both nutritional status and adequacy of nutritional rehabilitation. For these indications, IGF-I measurement is more sensitive and more specific than measurement of the other nutrient-related serum proteins (albumin, prealbumin, transferrin, retinol-binding protein). Animal models have been developed to investigate the mechanisms responsible for the nutritional regulation of IGF-I. There is no doubt that many mechanisms are involved (Fig. 12). Decline of serum IGF-I in dietary restriction is independent of the diet-induced alterations in pituitary GH secretion. The role of the liver GH receptors is dependent on the severity of the nutritional insult. In severe dietary restriction (fasting), a marked decrease of the number of somatogenic receptors supports the role of a receptor defect in the decline of circulating IGF-I. In contrast, in less severe forms of dietary restriction (protein restriction), the decline of IGF-I results from a postreceptor defect in the GH action at the hepatic level. Nutritional deprivation decreases hepatic IGF-I production by diminishing IGF-I gene expression. Decline in IGF-I gene expression is mainly caused by nutrient deficiency and less importantly by the nutritionally induced hormonal changes (insulin and T3). Diet restriction also increases the clearance and degradation of serum IGF-I through changes in the levels of circulating IGFBPs.(ABSTRACT TRUNCATED AT 400 WORDS)