Milner R D, Hill D J
Clin Endocrinol (Oxf). 1984 Oct;21(4):415-33. doi: 10.1111/j.1365-2265.1984.tb03229.x.
Both insulin and the related peptides, the insulin-like growth factors/somatomedins, may function as anabolic factors in the regulation of fetal body size. Infants born to women suffering from diabetes mellitus may show increased deposition of subcutaneous fat and enhanced lean body mass, findings reproduced in experimental animal fetuses with induced hyperinsulinaemia. Fetal adiposity may be associated with a life-time tendency to obesity and its associated diseases. Insulin-like growth factors I (IGFI) and II are present in the circulation of the newborn infant and animal fetus and correlate positively with birth size. The fetal tissues are biologically responsive to IGFs in vitro and are rich in specific cell membrane receptors, those predominantly recognizing IGFI being structurally and functionally similar to the insulin receptor. Insulin could theoretically influence fetal tissues by an interaction with either the insulin or IGF receptor. IGF release is a property of multiple fetal tissues in vitro, but, in contrast to postnatal life, is not dependent on growth hormone. Fetal IGF production may be influenced by placental lactogen, especially IGFII which rapidly declines in the circulation following parturition in the rat and sheep. A positive association also exists between circulating levels of insulin and IGFs when the former is experimentally manipulated in the animal fetus. Similarly the infant born with transient diabetes mellitus has low cord blood levels of insulin and IGFI. Insulin has a dual role in prenatal life. In the last trimester insulin functions as a glucoregulatory hormone, but from much earlier in gestation creates an anabolic environment in the fetus supplied with optimal nutrients. This latter mechanism of action is unclear and probably heterogeneous, but in overview is permissive rather than obligatory. In contrast the growth-promoting role of the IGFs is direct but their interaction with fetal tissues, and thus the overall emphasis of fetal growth, may be paracrine.
胰岛素及相关肽类，即胰岛素样生长因子/生长调节素，在调节胎儿体型方面可能发挥合成代谢因子的作用。患有糖尿病的女性所生婴儿可能会出现皮下脂肪沉积增加和瘦体重增加的情况，在实验诱导的高胰岛素血症动物胎儿中也会出现类似的结果。胎儿肥胖可能与一生的肥胖倾向及其相关疾病有关。胰岛素样生长因子I（IGF-I）和II存在于新生儿和动物胎儿的循环中，与出生体重呈正相关。胎儿组织在体外对IGF具有生物学反应，并且富含特定的细胞膜受体，主要识别IGF-I的受体在结构和功能上与胰岛素受体相似。理论上，胰岛素可通过与胰岛素或IGF受体相互作用来影响胎儿组织。IGF的释放是多种胎儿组织在体外的特性，但与出生后不同，它不依赖于生长激素。胎儿IGF的产生可能受胎盘催乳素的影响，尤其是IGF-II，在大鼠和绵羊分娩后，其在循环中的水平会迅速下降。当在动物胎儿中通过实验操纵胰岛素水平时，胰岛素和IGF的循环水平之间也存在正相关。同样，患有短暂性糖尿病的婴儿脐带血中的胰岛素和IGF-I水平较低。胰岛素在产前生活中具有双重作用。在妊娠晚期，胰岛素作为一种血糖调节激素发挥作用，但在妊娠早期就为胎儿创造了一个营养充足的合成代谢环境。后一种作用机制尚不清楚，可能具有异质性，但总体而言是允许性的而非强制性的。相比之下，IGF的促生长作用是直接的，但其与胎儿组织的相互作用以及胎儿生长的总体重点可能是旁分泌性的。
