title: Effects of glucose on placental hormones in the human term placenta in vitro.
abstract: Glucose intake during pregnancy results in a decrease in endogenous insulin-like growth factor binding protein-1 (IGFBP-1). However, the exact role of glucose on placental secretion of IGFBP-1 is unclear. This study 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 for an isolated human placenta lobule, a total of 43 experiments were performed over a duration of 6 hours. Twenty placentae were perfused with 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-like growth factor (IGF-I), IGFBP-1, human placental lactogen (hPL) and beta-human chorionic gonadotropin (beta-hCG) were measured at 30 minute intervals during perfusion. Insulin and IGF-I were barely detectable in the perfusates and their levels were not modulated by glucose. IGFBP-1 was predominantly detected in the maternal rather than the fetal compartment of the placental circulation. Glucose increased the levels of IGFBP-1 in the maternal circulation in groups I and II during the first two hours of perfusion (188 +/- 58% and 193 +/- 31%, respectively). However, during the subsequent 4 hour period, the increase in IGFBP-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, may be due to a lack of circulatory maternal insulin in the isolated placental preparation. These results also suggest that there may be a functional barrier within the placenta that prevents an increase in the level of IGFBP-1 in the fetal circulation.
authors.affiliation: Department of Obstetrics and Gynecology, Chang Gung Medical College and Hospital, Taipei, Taiwan ROC.
authors.forename: T T
authors.initials: TT
authors.lastname: Hsieh
authors.forename: K C
authors.initials: KC
authors.lastname: Chen
authors.forename: J J
authors.initials: JJ
authors.lastname: Hsu
authors.forename: T H
authors.initials: TH
authors.lastname: Chiu
authors.forename: C C
authors.initials: CC
authors.lastname: Hsieh
authors.forename: H S
authors.initials: HS
authors.lastname: Wang
mesh_terms: D018997:Chorionic Gonadotropin, beta Subunit, Human / Q000096:biosynthesis; D005260:Female; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D007328:Insulin / Q000096:biosynthesis; D018970:Insulin-Like Growth Factor Binding Protein 1 / Q000096:biosynthesis; D007334:Insulin-Like Growth Factor I / Q000096:biosynthesis; D019344:Lactic Acid / Q000378:metabolism; D010920:Placenta / Q000378:metabolism*; D010926:Placental Hormones / Q000096:biosynthesis*; D010928:Placental Lactogen / Q000096:biosynthesis; D011247:Pregnancy
chemical_list: D018997:Chorionic Gonadotropin, beta Subunit, Human; D007328:Insulin; D018970:Insulin-Like Growth Factor Binding Protein 1; D010926:Placental Hormones; D019344:Lactic Acid; D007334:Insulin-Like Growth Factor I; D010928:Placental Lactogen; D005947:Glucose