Glucose is one of the main nutrients for fetal development. Nevertheless, a significant gluconeogenesis ability by the fetus has not been reported, therefore the fetal glucose homeostasis depends on the ability of the placenta to carry out glucose from the maternal blood and to transport it to fetal tissues by means of specific transport molecules, known as GLUTs. Several conditions contribute to an imbalance in fetal glucose homeostasis, including incorrect mother feeding, maternal obesity, maternal type II diabetes and/or pregnancy complications. These conditions can affect the normal development of the fetus by affecting glucose transfer through the placenta. Nowadays it is known that environmental contaminants are able to impair placental glucose homeostasis compromising fetal development. These substances include synthetic chemicals with estrogen-like behavior referred as to Endocrine Disrupting Chemicals (EDCs), of which Bisphenol A represents one of the most important for its wide distribution in many daily-use products. However, in which way these two possible maternal perturbations (altered glucose supply and BPA exposure) are able to interfere with placental glucose uptake and how this interference may reflect on an incorrect fetal development has to be elucidated. For this purpose, this study aimed to clarify the effect of such perturbations on human placental glucose homeostasis. The studies were conducted in vitro, in human placental cell line, and in vivo, in rat placenta and fetal heart. The results showed that both, altered glucose supply and BPA exposure, influence human and rat placental glucose transport. Moreover, the in vivo study revealed that BPA disruption on placental glucose homeostasis compromise fetal rat heart development.

Benincasa, L. (2019). Placental responses to maternal perturbations: altered glucose homeostasis and Bisphenol A exposure.

Placental responses to maternal perturbations: altered glucose homeostasis and Bisphenol A exposure

Linda Benincasa
2019-01-01

Abstract

Glucose is one of the main nutrients for fetal development. Nevertheless, a significant gluconeogenesis ability by the fetus has not been reported, therefore the fetal glucose homeostasis depends on the ability of the placenta to carry out glucose from the maternal blood and to transport it to fetal tissues by means of specific transport molecules, known as GLUTs. Several conditions contribute to an imbalance in fetal glucose homeostasis, including incorrect mother feeding, maternal obesity, maternal type II diabetes and/or pregnancy complications. These conditions can affect the normal development of the fetus by affecting glucose transfer through the placenta. Nowadays it is known that environmental contaminants are able to impair placental glucose homeostasis compromising fetal development. These substances include synthetic chemicals with estrogen-like behavior referred as to Endocrine Disrupting Chemicals (EDCs), of which Bisphenol A represents one of the most important for its wide distribution in many daily-use products. However, in which way these two possible maternal perturbations (altered glucose supply and BPA exposure) are able to interfere with placental glucose uptake and how this interference may reflect on an incorrect fetal development has to be elucidated. For this purpose, this study aimed to clarify the effect of such perturbations on human placental glucose homeostasis. The studies were conducted in vitro, in human placental cell line, and in vivo, in rat placenta and fetal heart. The results showed that both, altered glucose supply and BPA exposure, influence human and rat placental glucose transport. Moreover, the in vivo study revealed that BPA disruption on placental glucose homeostasis compromise fetal rat heart development.
2019
Benincasa, L. (2019). Placental responses to maternal perturbations: altered glucose homeostasis and Bisphenol A exposure.
Benincasa, Linda
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/1071631
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo