c-peptide and Fetal-Hypoxia

Fifty-five pregnant Rhesus isoimmunized women were subjected to fetal blood sampling or fetal blood transfusion on 135 occasions. Glucose and C-peptide concentrations were measured in fetal blood, in addition to the routine investigations for complete blood count, blood gases and lactate concentration, in order to investigate whether fetal insulin secretion was affected by hypoxia from fetal anemia. We found a strong relation between the concentration of C-peptide and gestational age at sampling (r = 0.53, P less than or equal to 0.000001). Multiple regression analysis also demonstrated that glucose (P less than or equal to 0.0051) and lactate (P less than or equal to 0.0003) also affected the concentration of C-peptide. We were unable to find any relation between C-peptide concentrations and blood gas variables. We conclude that fetal insulin secretion, measured as C-peptide concentration in fetal blood, is not affected by hypoxia from anemia as long as hemoglobin concentration remains within the range 2.1-14.8 g/dl).

Topics: Age Factors; Blood Glucose; C-Peptide; Carbon Dioxide; Erythroblastosis, Fetal; Female; Fetal Blood; Fetal Hypoxia; Fetus; Gestational Age; Humans; Hydrogen-Ion Concentration; Infant, Newborn; Insulin; Insulin Secretion; Lactates; Lactic Acid; Oxygen; Pregnancy; Regression Analysis; Rh Isoimmunization

Nonhuman primate models of gestational diabetes have produced fetopathies most similar to those of the human infant of the mother with gestational diabetes (IGDM). Fetal hyperglycemia, hyperinsulinemia, macrosomia, selective organomegaly, intrauterine death, and placental hyperplasia are hallmarks of the fetopathy of the IGDM. The chronic infusion of insulin into the fetus of a normal pregnant rhesus monkey results in fetal hyperinsulinemia with normal to low plasma metabolic substrate concentrations. Under these conditions, fetal hyperinsulinemia is sufficient to cause fetal growth and hormone changes observed in the human IGDM. Our studies provide evidence that the soft tissue hyperplasia in the fetal macrosomia syndromes in humans and nonhuman primates in which fetal hyperinsulinemia is observed is the direct result of that chronic in utero hyperinsulinemia.

Topics: Adipose Tissue; Amino Acids; Animals; Birth Weight; Blood Glucose; C-Peptide; Disease Models, Animal; Erythropoietin; Female; Fetal Blood; Fetal Hypoxia; Fetus; Glucagon; Hydrocortisone; Insulin; Macaca mulatta; Pregnancy; Pregnancy in Diabetics