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Obesity and Preeclampsia: Common Pathophysiological Mechanisms

Preeclampsia is a disorder specific of the human being that appears after 20 weeks of pregnancy, characterized by new onset of hypertension and proteinuria. Abnormal placentation and reduced placental perfusion associated to impaired trophoblast invasion and alteration in the compliance of uterine s...

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Autores principales: Lopez-Jaramillo, Patricio, Barajas, Juan, Rueda-Quijano, Sandra M., Lopez-Lopez, Cristina, Felix, Camilo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6305943/
https://www.ncbi.nlm.nih.gov/pubmed/30618843
http://dx.doi.org/10.3389/fphys.2018.01838
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author Lopez-Jaramillo, Patricio
Barajas, Juan
Rueda-Quijano, Sandra M.
Lopez-Lopez, Cristina
Felix, Camilo
author_facet Lopez-Jaramillo, Patricio
Barajas, Juan
Rueda-Quijano, Sandra M.
Lopez-Lopez, Cristina
Felix, Camilo
author_sort Lopez-Jaramillo, Patricio
collection PubMed
description Preeclampsia is a disorder specific of the human being that appears after 20 weeks of pregnancy, characterized by new onset of hypertension and proteinuria. Abnormal placentation and reduced placental perfusion associated to impaired trophoblast invasion and alteration in the compliance of uterine spiral arteries are the early pathological findings that are present before the clinical manifestations of preeclampsia. Later on, the endothelial and vascular dysfunction responsible of the characteristic vasoconstriction of preeclampsia appear. Different nutritional risk factors such as a maternal deficit in the intake of calcium, protein, vitamins and essential fatty acids, have been shown to play a role in the genesis of preeclampsia, but also an excess of weight gain during pregnancy or a pre-pregnancy state of obesity and overweight, which are associated to hyperinsulinism, insulin resistance and maternal systemic inflammation, are proposed as one of the mechanism that conduce to endothelial dysfunction, hypertension, proteinuria, thrombotic responses, multi-organ damage, and high maternal mortality and morbidity. Moreover, it has been demonstrated that pregnant women that suffer preeclampsia will have an increased risk of future cardiovascular disease and related mortality in their later life. In this article we will discuss the results of studies performed in different populations that have shown an interrelationship between obesity and overweight with the presence of preeclampsia. Moreover, we will review some of the common mechanisms that explain this interrelationship, particularly the alterations in the L-arginine/nitric oxide pathway as a crucial mechanism that is common to obesity, preeclampsia and cardiovascular diseases.
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spelling pubmed-63059432019-01-07 Obesity and Preeclampsia: Common Pathophysiological Mechanisms Lopez-Jaramillo, Patricio Barajas, Juan Rueda-Quijano, Sandra M. Lopez-Lopez, Cristina Felix, Camilo Front Physiol Physiology Preeclampsia is a disorder specific of the human being that appears after 20 weeks of pregnancy, characterized by new onset of hypertension and proteinuria. Abnormal placentation and reduced placental perfusion associated to impaired trophoblast invasion and alteration in the compliance of uterine spiral arteries are the early pathological findings that are present before the clinical manifestations of preeclampsia. Later on, the endothelial and vascular dysfunction responsible of the characteristic vasoconstriction of preeclampsia appear. Different nutritional risk factors such as a maternal deficit in the intake of calcium, protein, vitamins and essential fatty acids, have been shown to play a role in the genesis of preeclampsia, but also an excess of weight gain during pregnancy or a pre-pregnancy state of obesity and overweight, which are associated to hyperinsulinism, insulin resistance and maternal systemic inflammation, are proposed as one of the mechanism that conduce to endothelial dysfunction, hypertension, proteinuria, thrombotic responses, multi-organ damage, and high maternal mortality and morbidity. Moreover, it has been demonstrated that pregnant women that suffer preeclampsia will have an increased risk of future cardiovascular disease and related mortality in their later life. In this article we will discuss the results of studies performed in different populations that have shown an interrelationship between obesity and overweight with the presence of preeclampsia. Moreover, we will review some of the common mechanisms that explain this interrelationship, particularly the alterations in the L-arginine/nitric oxide pathway as a crucial mechanism that is common to obesity, preeclampsia and cardiovascular diseases. Frontiers Media S.A. 2018-12-19 /pmc/articles/PMC6305943/ /pubmed/30618843 http://dx.doi.org/10.3389/fphys.2018.01838 Text en Copyright © 2018 Lopez-Jaramillo, Barajas, Rueda-Quijano, Lopez-Lopez and Felix. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Lopez-Jaramillo, Patricio
Barajas, Juan
Rueda-Quijano, Sandra M.
Lopez-Lopez, Cristina
Felix, Camilo
Obesity and Preeclampsia: Common Pathophysiological Mechanisms
title Obesity and Preeclampsia: Common Pathophysiological Mechanisms
title_full Obesity and Preeclampsia: Common Pathophysiological Mechanisms
title_fullStr Obesity and Preeclampsia: Common Pathophysiological Mechanisms
title_full_unstemmed Obesity and Preeclampsia: Common Pathophysiological Mechanisms
title_short Obesity and Preeclampsia: Common Pathophysiological Mechanisms
title_sort obesity and preeclampsia: common pathophysiological mechanisms
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6305943/
https://www.ncbi.nlm.nih.gov/pubmed/30618843
http://dx.doi.org/10.3389/fphys.2018.01838
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