Repositorio de producción científica de la Universidad de Sevilla

Akt/mTOR Role in Human Foetoplacental Vascular Insulin Resistance in Diseases of Pregnancy

Opened Access Akt/mTOR Role in Human Foetoplacental Vascular Insulin Resistance in Diseases of Pregnancy

Citas

buscar en

Estadísticas
Icon
Exportar a
Autor: Villalobos Labra, Roberto
Silva, Luis Felipe
Subiabre, Mario
Araos, Joaquín
Salsoso Rodríguez, Rocío
Sobrevia Luarte, Luis
Departamento: Universidad de Sevilla. Departamento de Fisiología
Fecha: 2017
Publicado en: Journal of Diabetes Research, 5947859, 1-13.
Tipo de documento: Artículo
Resumen: Insulin resistance is characteristic of pregnancies where the mother shows metabolic alterations, such as preeclampsia (PE) and gestational diabetes mellitus (GDM), or abnormal maternal conditions such as pregestational maternal obesity (PGMO). Insulin signalling includes activation of insulin receptor substrates 1 and 2 (IRS1/2) as well as Src homology 2 domain-containing transforming protein 1, leading to activation of 44 and 42 kDa mitogen-activated protein kinases and protein kinase B/Akt (Akt) signalling cascades in the human foetoplacental vasculature. PE, GDM, and PGMO are abnormal conditions coursing with reduced insulin signalling, but the possibility of the involvement of similar cell signalling mechanisms is not addressed. This review aimed to determine whether reduced insulin signalling in PE, GDM, and PGMO shares a common mechanism in the human foetoplacental vasculature. Insulin resistance in these pathological conditions results from reduced Akt activation mainly due to...
[Ver más]
Cita: Villalobos Labra, R., Silva, L.F., Subiabre, M., Araos, J., Salsoso Rodríguez, R. y Sobrevia Luarte, L. (2017). Akt/mTOR Role in Human Foetoplacental Vascular Insulin Resistance in Diseases of Pregnancy. Journal of Diabetes Research, 5947859, 1-13.
Tamaño: 980.7Kb
Formato: PDF

URI: https://hdl.handle.net/11441/70198

DOI: 10.1155/2017/5947859

Ver versión del editor

Mostrar el registro completo del ítem


Esta obra está bajo una Licencia Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 Internacional

Este registro aparece en las siguientes colecciones