Fowden A L
Physiological Laboratory, Cambridge, UK.
Early Hum Dev. 1992 Jun-Jul;29(1-3):177-81. doi: 10.1016/0378-3782(92)90135-4.
Disturbances in fetal insulin secretion are associated with abnormalities in fetal growth in a variety of species: excessive insulin secretion can lead to fetal macrosomia while fetal hypoinsulinaemia invariably causes fetal growth retardation. Fetal insulin deficiency caused by pancreatectomy (PX) of the sheep fetus leads to reduced body weight, crown-rump length and limb lengths at delivery near term. The growth rate in utero fell by 40-50% after PX and could be restored to normal values by insulin replacement treatment. These changes in growth were accompanied by reductions of 30-40% in the rates of umbilical uptake, utilization and oxidation of glucose by the sheep fetus. Insulin is therefore a physiological regulator of fetal growth and acts in part by stimulating the cellular uptake of glucose and its preferential use for oxidative metabolism in the fetal tissues.
在多种物种中，胎儿胰岛素分泌紊乱与胎儿生长异常有关：胰岛素分泌过多会导致胎儿巨大儿，而胎儿低胰岛素血症总是会导致胎儿生长受限。绵羊胎儿胰腺切除术（PX）导致的胎儿胰岛素缺乏会使足月分娩时体重、顶臀长度和肢体长度降低。PX后子宫内生长速率下降40 - 50%，通过胰岛素替代治疗可恢复到正常水平。这些生长变化伴随着绵羊胎儿脐部葡萄糖摄取、利用和氧化速率降低30 - 40%。因此，胰岛素是胎儿生长的生理调节因子，部分作用是通过刺激胎儿组织对葡萄糖的细胞摄取及其优先用于氧化代谢。
