Glucose gradients of maternal vein-umbilical vein and umbilical vein-umbilical artery in normally grown and growth-retarded fetuses.J Perinat Med 1991; 19(6):421-5JP
The present study was designed to investigate the roles of maternal-fetal glucose transport and fetal glucose utilization in the regulation of fetal growth. Maternal venous blood, umbilical arterial and venous blood were sampled simultaneously in 60 full-term appropriate-for gestational age (AGA) fetuses and 48 small-for-gestational-age (SGA) fetuses. The cases were divided into four groups: group 1 consisted of 35 AGA fetuses, group 2 consisted of 25 AGA fetuses, group 3 consisted of 25 SGA fetuses, and group 4 consisted of 22 SGA fetuses. The mothers of group 1 and 3 were given 2.5% glucose in 0.9% normal saline and those of groups 2 and 4 by cesarean section received normal saline or Ringer's lactate at least one hour prior to delivery of the fetus SGA fetuses were found to have hypoglycaemia of umbilical venous blood, increased (maternal vein-umbilical vein) MV-UV and decreased UV-UA (umbilical vein-umbilical artery) glucose gradients, all of which disappeared after maternal glucose supplementation. However, hypoinsulinemia and lower insulin/glucose ratio in SGA fetuses persisted either with or without maternal parenteral glucose infusion. Increased MV-UV and decreased UV-UA glucose gradients suggests placental dysfunction and poor glucose utilization in SGA fetuses. The lower fetal insulin/glucose ratio may imply pancreatic dysfunction in SGA fetuses, which did not respond to glucose challenge from the maternal side. It seems that in SGA fetuses, placental dysfunction interferes with maternal-fetal transfer with resulting fetal hypoglycemia; on the other hand, pancreatic dysfunction leads to poor glucose utilization and retarded intrauterine growth. However, the mechanism that primarily accounts for pancreatic dysfunction in these fetuses remains to be resolved.