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Endocrine pancreatic function in growth-retarded fetuses
C Hubinont1, U Nicolini, N M Fisk
1Institute of Obstetrics and Gynecology, Royal Postgraduate Medical School, London, United Kingdom.
Insights
Fetal growth restriction is linked to altered glucose metabolism. Elevated fetal glucagon may indicate fetal compromise, offering a better indicator than glucose or insulin levels.
Area of Science:
- Perinatal Medicine
- Endocrinology
- Fetal Physiology
Background:
- Fetal growth restriction (FGR) impacts neonatal outcomes.
- Understanding metabolic adaptations in FGR is crucial for clinical management.
Purpose of the Study:
- To investigate maternal-fetal glucose dynamics and fetal hormonal profiles in FGR.
- To assess the utility of fetal glucose, insulin, and glucagon as indicators of fetal compromise.
Main Methods:
- Measured maternal-fetal glucose gradient, fetal plasma glucose, insulin, and glucagon in 63 fetuses (34 controls, 29 FGR).
- Subdivided FGR group based on umbilical artery end-diastolic frequencies.
Main Results:
- Growth-retarded fetuses exhibited higher maternal-fetal glucose gradients and fetal glucagon, but lower fetal glucose and insulin compared to controls.
- Within the FGR group, fetuses without end-diastolic frequencies had elevated fetal glucagon.
- Fetal glucagon levels correlated with indicators of fetal compromise.
Conclusions:
- Increased fetal glucagon in FGR may represent a compensatory response to hypoglycemia.
- Fetal glucagon appears to be a more sensitive marker of fetal compromise in FGR than fetal glucose or insulin.
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.