RT info:eu-repo/semantics/article
T1 Excess hydrocortisone hampers placental nutrient uptake disrupting cellular metabolism
A1 Mateos, Rosa María .
A1 Jiménez, Gema .
A1 Álvarez Gil, Carmen .
A1 Visiedo, Francisco .
A1 Rivera Rodríguez, Fátima .
A1 Santos Rosendo, Celeste .
A1 Rodríguez Pareja, Antonia .
A1 Perdomo Hernández, Germán M.
A1 Lechuga Sancho, Alfonso .
K1 Endocrinología
K1 Endocrinology
K1 Obstetricia
K1 Obstetrics
AB Low birth weight increases neonatal morbidity and mortality, and surviving infants have increased risk of metabolic andcardiovascular disturbances later in life, as well as other neurological, psychiatric, and immune complications. A gestationalexcess of glucocorticoids (GCs) is a well-known cause for fetal growth retardation, but the biological basis for this associationremains elusive. Placental growth is closely related to fetal growth. The placenta is the main regulator of nutrient transport tothe fetus, resulting from the difference between placental nutrient uptake and the placenta’s own metabolism. The aim of thisstudy was to analyze how excess hydrocortisone affects placental glucose and lipid metabolism. Human placenta explants fromterm physiological pregnancies were cultured for 18 hours under different hydrocortisone concentrations (2.75, 5.5, and 55mM;1, 2, and 20mg/ml). Placental glucose and lipid uptake and the metabolic partitioning of fatty acids were quantified by isotopictechniques, and expression of specific glucose transporterGLUT1was quantified bywestern blot.Cell viabilitywas assessed byMTT,immunohistochemistry and caspase activity. We found that excess hydrocortisone impairs glucose uptake and lipoprotein lipase(LPL) activity, coincident with a GC-dose dependent inhibition of fatty acid oxidation and esterification. None of the experimentalconditions showed an increased cell death. In conclusion, our results show that GC overexposure exerts a dysfunctional effect onlipid transport and metabolism and glucose uptake in human placental explants. These findings could well be directly related toa reduced placental growth and possibly to a reduced supply of nutrients to the fetus and the consequent fetal growth retardationand metabolic programming.
PB Hindawi Publishing Corporation
SN 2314-6133
YR 2018
FD 2018
LK http://hdl.handle.net/10259/4974
UL http://hdl.handle.net/10259/4974
LA eng
DS Repositorio Institucional de la Universidad de Burgos
RD 28-abr-2024