RADIOIMMUNOLOGICAL DETERMINATION OF INSULIN-LIKE GROWTH FACTORS-I AND FACTORS-II IN NORMAL SUBJECTS AND IN PATIENTS WITH GROWTH DISORDERS AND EXTRA-PANCREATIC TUMOR HYPOGLYCEMIA
RADIOIMMUNOLOGICAL DETERMINATION OF INSULIN-LIKE GROWTH FACTORS-I AND FACTORS-II IN NORMAL SUBJECTS AND IN PATIENTS WITH GROWTH DISORDERS AND EXTRA-PANCREATIC TUMOR HYPOGLYCEMIA
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DOI：
10.1172/jci110379
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发表时间：
1981-01-01
影响因子：
15.9
通讯作者：
FROESCH, ER
中科院分区：
文献类型：
--
作者：
ZAPF, J;WALTER, H;FROESCH, ER
免疫反应性胰岛素样生长因子（IGF）I和II的血清水平测定了一个修改的IGF I和一个新的IGF II放射免疫分析法在正常儿童和成人，并在肢端肥大症，孤立的生长激素缺乏症和胰腺外肿瘤低血糖症患者。通过简单的常规程序在酸性pH下对血清样品进行凝胶过滤，以使IGF与IGF载体蛋白解离和分离。平均免疫反应性IGF I水平（±. SD;校正IGF II的交叉反应性）为193 ± 0.01。正常成人受试者为58 ng/ml，712 . ±.肢端肥大症患者为245 ng/ml，单纯性生长激素缺乏症患者为14 ng/ml。生长激素单独缺乏，不管其他正常的激素状态，似乎是负责IGF I水平急剧下降。生长激素的过度分泌不增加免疫反应性IGF II的水平：平均水平（. ±. SD;校正IGF I的交叉反应性）在正常和肢端肥大症受试者中实际上是相同的（647 . ±. 126和641 .+-. 189 ng/ml）。显然，正常的生长激素水平已经最大限度地刺激IGF II的产生。在生长激素缺乏症中，免疫反应性IGF II显著降低（252 . ±. 99 ng/ml）。因此，IGF II，像IGF I一样，是生长激素依赖性的。但与IGF I相反，IGF II的生长激素依赖性似乎仅在低于正常的生长激素水平时才变得明显。在正常儿童中，IGF I是年龄依赖性的：它在新生儿脐带血清中较低（51 . ±. 20 ng/ml），并随着年龄的增长逐渐上升到成人范围。在青春期开始和青春期期间，平均IGF I水平高于青春期前的值。相反，正常儿童的IGF II水平与年龄和青春期阶段无关，而新生儿的IGF II值明显较低。胰腺外肿瘤引起的低血糖与免疫反应性IGF I或II水平升高无关。IGF I在大多数血清中降低（平均水平± 0.0001）。标准差：56 ±。39 ng/ml），而IGF II处于正常范围（556 ± 0.39ng/ml）。195 ng/ml）。
Serum levels of immunoreactive insulin-like growth factors (IGF) I and II were determined by a modified IGF I and a new IGF II radioimmunoassay in normal children and adults, and in patients with acromegaly, isolated growth hormone deficiency and extrapancreatic tumor hypoglycemia. Serum samples were gel filtered by a simple routine procedure at acidic pH to dissociate and separate IGF from the IGF carrier protein. Mean immunoreactive IGF I levels (.+-. SD; corrected for crossreactivity of IGF II) were 193 .+-. 58 ng/ml in normal adult subjects, 712 .+-. 245 ng/ml in acromegalic patients and 24 .+-. 14 ng/ml in patients with isolated growth hormone deficiency. The lack of growth hormone alone, irrespective of an otherwise normal hormonal status, appears to be responsible for the drastic decrease of IGF I levels. Oversecretion of growth hormone does not increase the levels of immunoreactive IGF II: mean levels (.+-. SD; corrected for crossreactivity of IGF I) in normal and acromegalic subjects are virtually identical (647 .+-. 126 and 641 .+-. 189 ng/ml, respectively). Apparently, normal growth hormone levels stimulate IGF II production already maximally. In growth hormone deficiency immunoreactive IGF II is significantly decreased (252 .+-. 99 ng/ml). Thus, IGF II, like IGF I, is growth hormone dependent. But in contrast to IGF I, the growth hormone dependence of IGF II seems to become apparent only at subnormal growth hormone levels. In normal children IGF I is age dependent: it is low in newborn cord sera (51 .+-. 20 ng/ml) and gradually rises into the adult range with increasing age. At the onset of and during puberty mean IGF I levels lie above prepubertal values. In contrast, IGF II levels in normal children are independent of age and pubertal stage beyond the 1st year of life, whereas newborns have significantly lower IGF II values. Hypoglycemia resulting from extrapancreatic tumors is not associated with increased immunoreactive IGF I or II levels. IGF I is decreased in most of the sera (mean level .+-. SD: 56 .+-. 39 ng/ml) whereas IGF II lies in the normal range (556 .+-. 195 ng/ml).