Changes in aquaporin 1 expression affect amniotic fluid volume

Abstract

STEPHANIE MANN, NATALIA DVORAK, ROBERT TAYLOR, Phoenix Integrated Residency in Ob/Gyn, Obstetrics and Gynecology, Phoenix, Arizona, University of California, San Francisco, Obstetrics, Gynecology and Reproductive Sciences, San Francisco, California OBJECTIVE: Recent work from our laboratory has demonstrated the presence of aquaporin (AQP) water channels in fetal membranes from pregnancies with normal amniotic fluid (AF) volume. The objective of this study was to investigate changes in AQP 1 mRNA expression from fetal membranes of pregnancies with polyhydramnios and oligohydramnios. STUDY DESIGN: Placentas from term pregnancies (37-40 wks) were collected from women who presented with intact membranes and one of the following: (1) idiopathic oligohydramnios (AFI !5.0 cm); (2) polyhydramnios (AFI >24.0 cm); and (3) normal amount AF (AFI >5.0 cm and!24.0 cm). The membranes (amnion and chorion) directly overlying the placenta and the free floating reflected membranes were sampled (total of four samples from each placenta). RNA was isolated from the amnion and chorion of each region. Quantitative RT-PCR was used to compare expression of AQP1 mRNA in the membranes collected from the above pregnancies. Statistical analysis was performed with a t test. P ! .05 was considered signficant. RESULTS: As shown in the figure, AQP1 mRNA expression is increased in the reflected amnion from pregnancies with idiopathic polyhydramnios and decreased in the reflected amnion and chorion from pregnancies with oligohydramnios. CONCLUSION: The expression of the water channel AQP1 is altered in the reflected fetal membranes. These results suggests that there is an adaptive response by the fetal membranes in situations of either decreased or increased AF volume to prevent excessive loss or accumulation of fluid, respectively. We speculate that therapies focused on regulating AQP1 expression may be useful for treating oligohydramnios and polyhydramnios. 458 PERINATAL GLUCOSE TOLERANCE AFTER INTRAUTERINE GROWTH RESTRICTION IN THE LATE-GESTATION OVINE FETUS PHILIPPE DERUELLE, IVA GUEORGUIEVA, BERENGERE SICOT DE JENLIS, SOPHIE JAILLARD, JACQUES WEILL, VERONIQUE DEBARGE, LAURENT STORME, CHRU de Lille, Lille, France, CHRU de Lille, Pediatric endocrinology unit, Lille, France, CHRU de Lille, Department of perinatology, Lille, France, CHRU de Lille, France, Department of perinatology, Lille, France OBJECTIVE: Newborns with Intrauterine-Growth Restriction (IUGR) are at increased risk to develop a metabolic syndrome later in life, namely obesity, cardiovascular disease, impaired glucose tolerance. Whereas these facts have been largely studied during childhood or adult life, little is known about the consequences of IUGR on glucose tolerance during the perinatal period. The purpose of this study was to determine whether chronic placental embolization in the late gestation ovine fetus induce insulin resistance during the perinatal period. STUDY DESIGN: IUGR was induced by umbilico-placental embolization during late gestation in chronically catheterized sheep. Umbilico-placental embolization was performed between 130 and 140 d of gestation (terme = 147 d) during which fetuses were hypoxemic relative to controls. Euglycemic, hyperinsulinemic glucose clamp experiments were performed in utero and during the first three weeks after birth in order to measure the effect of fetal insulin concentration on fetal glucose uptake at a constant glucose concentration. Fetal coricotropin, cortisol and catecholamines concentrations were measured daily. RESULTS: Chronic placental embolization produced asymmetrically IUGR fetuses and increased vascular resistance in umbilical artery (P ! .05). The exogenous glucose infusion rate necessary to maintain constant glycemia was significantly lower in IUGR relative to control fetuses at 140 d of gestation (IUGR vs. control, 2.5 G .5 mg/kg/min and 5.0 G 0.5 mg/kg/min, P ! .05) and 7 days after birth (IUGR vs. control, 3.5 G .7 mg/kg/min and 5.7 G 1.4 mg/kg/ min, P ! .05). Glucose clamps were similar between groups at 2 and 3 weeks after birth. Cortisol levels were similar between the two groups. In response to chronic fetal hypoxemia, there was a progressive increased in baseline fetal plasma epinephrine, norepinephrine and dopamine concentrations (P ! .01). CONCLUSION: We concluded that chronic fetal hypoxemia induces insulin resistance during the perinatal period. We speculate that this change could be related to an increase in fetal catecholamines levels.