Tk. Hytinantti et al., Increased fetal leptin in Type I diabetes mellitus pregnancies complicatedby chronic hypoxia, DIABETOLOG, 43(6), 2000, pp. 709-713
Aims/hypothesis. The purpose of this study was to examine whether fetal lep
tin concentration correlates with severity of chronic or subchronic fetal h
ypoxia as indicated by increased fetal concentrations of erythropoietin in
fetuses of mothers with Type I (insulin dependent) diabetes mellitus.
Methods. We measured leptin and erythropoietin concentrations in cord plasm
a and amniotic fluid with radioimmunoassay in 25 pregnancies (gestational a
ge 37.2 +/- 1.0 weeks). Fetuses with amniotic fluid erythropoietin over 22.
5 mU/ml were classified as hypoxic (n = 9) and those with amniotic fluid er
ythropoietin below 22.5 mU/ml (n = 16) as non-hypoxic.
Results. The hypoxic fetuses had significantly higher cord leptin concentra
tions than non-hypoxic fetuses (median 36.8; range, 12.5-135.1 vs median 16
.2; range, 3.7-52.2 mu g/l), (p = 0.0066). Cord plasma leptin (n = 25) corr
elated directly with amniotic fluid erythropoietin (r = 0.727, p = 0.0001),
with cord plasma erythropoietin (r = 0.644, p = 0.0005) and with the mater
nal last trimester HbA(1C) (r = 0.612, p = 0.0019) and negatively with cord
artery pO(2) (r = -0.440, p = 0.032), and pH (r = -0.414, p = 0.040).
Conclusion/interpretation. Fetal leptin concentrations increased concomitan
tly with erythropoietin during chronic or subchronic hypoxia. This phenomen
on could indicate a role for leptin in fetal adaptation to hypoxia.