Hill D E
Clin Obstet Gynecol. 1980 Sep;23(3):837-47.
The developing fetal endocrine pancrease produces both insulin and glucagon from an early stage in human development. These hormones do not cross the placenta and must be metabolized within the fetal-placental unit. Altered substrate metabolism in the gestational diabetic of the insulin dependent diabetic patient can pertubate normal fetal hormone homeostasis. Maternal hyperglycemia produces fetal hyperglycemia, hyperinsulinemia, and macrosomia while meticulous regulation of maternal glycemia abolishes the fetal macrosomia. Conversely, low levels of insulin or absence of fetal insulin results in fetal growth failure after 30 weeks' gestation. These examples, plus studies of the end-organ defects (receptors) in insulin metabolism, indicate that insulin is the major anabolic hormone of late fetal life. Glucagon appears to play less of a role in fetal life but has a homeostatic function in gluconeogenesis in the newborn. No specific growth-promoting role has been demonstrated for glucagon.
在人类发育的早期阶段，发育中的胎儿内分泌胰腺就开始分泌胰岛素和胰高血糖素。这些激素不会穿过胎盘，必须在胎儿 - 胎盘单位内进行代谢。胰岛素依赖型糖尿病患者妊娠期糖尿病患者的底物代谢改变会扰乱正常的胎儿激素稳态。母体高血糖会导致胎儿高血糖、高胰岛素血症和巨大儿，而对母体血糖的精确调节可消除胎儿巨大儿。相反，胰岛素水平低或胎儿胰岛素缺乏会导致妊娠30周后胎儿生长受限。这些例子，加上对胰岛素代谢中终末器官缺陷（受体）的研究，表明胰岛素是胎儿晚期主要的合成代谢激素。胰高血糖素在胎儿期的作用似乎较小，但在新生儿糖异生中具有稳态功能。尚未证明胰高血糖素有特定的促进生长作用。
