Endocrine pancreatic function in growth-retarded fetuses

Obstet Gynecol. 1991 Apr;77(4):541-4.

Abstract

Maternal-fetal glucose gradient and fetal plasma glucose, insulin, and glucagon were measured in 63 fetuses: 34 controls and 29 with growth retardation (nine with and 20 without end-diastolic frequencies in the umbilical artery). Maternal-fetal glucose gradient and fetal glucagon levels were higher in the growth-retarded group than in controls (P less than .001), whereas fetal insulin and glucose concentrations were lower (P less than .001). Although maternal-fetal glucose gradient, fetal glucose, and insulin concentrations were similar among the growth-retarded fetuses, fetuses without end-diastolic frequencies in the umbilical artery had higher fetal glucagon levels (P = .01) than those with end-diastolic frequencies. In growth-retarded fetuses, the increase in fetal glucagon might reflect a compensatory response to hypoglycemia and appears to be a better index of fetal compromise than is glucose or insulin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blood Glucose / analysis
  • Female
  • Fetal Blood / chemistry*
  • Fetal Growth Retardation / blood
  • Fetal Growth Retardation / physiopathology*
  • Glucagon / blood
  • Humans
  • Insulin / blood
  • Islets of Langerhans / physiopathology*
  • Pregnancy / blood

Substances

  • Blood Glucose
  • Insulin
  • Glucagon