EFFECTS OF GLUCOSE ON PLACENTAL HORMONES IN THE HUMAN TERM PLACENTA IN-VITRO

Glucose intake during pregnancy results in a decrease in endogenous in sulinlike growth factor binding protein-1 (IGFBP-1). However, the exac t role of glucose on placental secretion of IGFBP-1 is unclear. This s tudy was designed to investigate the direct effects of glucose on the production of IGFBP-1 and other placental hormones, using an isolated placental preparation. Using the dual recirculating perfusion system f or an isolated human placenta lobule, a total of 43 experiments were p erformed over a duration of 6 hours. Twenty placentae were perfused wi th a medium containing 141 +/- 10 mg/dL (7.83 +/- 0.56 mmol/L) glucose (group I) and 23 placentae with 242 +/- 12 mg/dL (13.43 +/- 0.67 mmol /L) glucose (group II). Levels of insulin, glucose, lactate, insulin-l ike growth factor (IGF-I), IGFBP-1, human placental lactogen (hPL) and beta-human chorionic gonadotropin (beta-hCG) were measured at 30 minu te intervals during perfusion. Insulin and IGF-I were barely detectabl e in the perfusates and their levels were not modulated by glucose. IG FBP-1 was predominantly detected in the maternal rather than the fetal compartment of the placental circulation. Glucose increased the level s of IGFBP-1 in the maternal circulation in groups I and II during the first two hours of perfusion (188 +/- 58% and 193 +/- 31%, respective ly). However, during the subsequent 4 hour period, the increase in IGF BP-1 concentration was significantly higher in group II (926 +/- 427%) than in group I (428 +/- 216%) (p < 0.05). There was no difference in the levels of hPL or beta-hCG between the two groups in the maternal circulation. Thus, glucose stimulates the production of IGFBP-1 in the maternal circulation of a placenta in vitro. This increase in IGFBP-1 by glucose in vitro, as opposed to the decrease of IGFBP-1 in vivo ma y be due to a lack of circulatory maternal insulin in the isolated pla cental preparation. These results also suggest that there may be a fun ctional barrier within the placenta that prevents an increase in the l evel of IGFBP-1 in the fetal circulation.