Abstract
The pathogenesis of congenital anomalies which are frequently observed in infants of diabetic mothers remains obscure. One possibility is that maternal insulin (I) may cross the placenta and act as a teratogen. Although at term the placenta is a barrier to I, this process has not been examined during organogenesis. To study this question, tracer amounts of radiolabelled I (I131 or I125) shown to contain 69-85% immunoreactive I were infused into 7 pregnant rate on day 12½ postcoitum (organogenesis: day 7-14) with a prime plus constant infusion. After 2 hrs maternal plasma and fetal and placental tissue were obtained. Plasma and tissue samples were analyzed for total radioactivity (TRA) as well as the radioactivity of the trichloroacetic acid protein precipitable fractions (TCA ppt). Significant TRA was achieved in maternal plasma at 2 hr: 3.2 − 3.4 × 103 and 3.9 − 5.8 × 104 cpm per 100 μl for I125 and I131, respectively. The percentage of the TRA in the TCA ppt was 59±7% (M±SD). This fraction contains the immunoreactive insulin fraction in addition to insulin polypeptide fragments. Placental tissue (containing some maternal blood) and fetal tissue had mean TCA ppt counts (per 100 mg) which were only 5.7% (0.7 − 16.5, range) and 0.05% (0 − 0.19) of the TCA ppt counts in maternal plasma. Since the fetus is protected from maternal insulin by the placenta during the period of late organogenesis, it is unlikely that maternal insulin acts as a fetal teratogen.
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