IQUIBICEN   23947
INSTITUTO DE QUIMICA BIOLOGICA DE LA FACULTAD DE CIENCIAS EXACTAS Y NATURALES
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
VIP-DEFICIENT mice pregnancies ehibit placental glucose uptake and transplacental transport alterations
Autor/es:
PAPARINI, DANIEL E.; WASCHEK, JAMES; HAUK, VANESA; RAMHORST, ROSANNA; MERECH, FÁTIMA; NAGUILA, ZAIRA; PÉREZ LEIRÓS, CLAUDIA
Reunión:
Congreso; SAIC-SAI-SAFIS; 2020
Resumen:
Adequate glucose uptake by trophoblast cells (Tb) is crucial to allow placental and fetal development. Placental metabolic alterations were reported in pregnancy complications and impairment of mTOR activity was observed in placentas with fetal growth restriction. Vasoactive Intestinal Peptide (VIP) has embryotrophic effects. We have recently shown its modulatory effect on Tb metabolism and we described a murine pregnancy model with VIP-deficient Tb cells presenting impaired placentation and reduced fetal weight at gestational day (gd) 14.5/17.5. VIP treatment at gd6.5 restored fetal weight. Our aim was to evaluate in vivo placental glucose uptake and transfer to the fetus in this model and the effect of VIP treatment on placental metabolism. We mated VIP+/+ females with VIP+/+ or VIP-/- males. For VIP treatment 2 nmol VIP were injected at gd6.5. At gd17.5 females were intraperitoneally injected with 3mM glucose fluorescent analogue 2-NBDG for 1.5h. Fluorescence of fetal/placental tissue was quantified in a fluorimeter. Placental/fetal GLUT1/mTOR expression was measured by RT-qPCR. For ex vivo experiments, VIP+/+ placental explants were incubated with VIP antagonist prior to the in vitro addition of 2-NBDG. We found that VIP antagonist impaired glucose uptake in placental explants (p