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Programming of Fetal Insulin Resistance in Pregnancies with Maternal Obesity by ER Stress and Inflammation

The global epidemics of obesity during pregnancy and excessive gestational weight gain (GWG) are major public health problems worldwide. Obesity and excessive GWG are related to several maternal and fetal complications, including diabetes (pregestational and gestational diabetes) and intrauterine pr...

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Published in:BioMed research international 2014-01, Vol.2014 (2014), p.1-13
Main Authors: Westermeier, Francisco, Sáez, Pablo J., Villalobos-Labra, Roberto, Sobrevia, Luis, Farías-Jofré, Marcelo
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description The global epidemics of obesity during pregnancy and excessive gestational weight gain (GWG) are major public health problems worldwide. Obesity and excessive GWG are related to several maternal and fetal complications, including diabetes (pregestational and gestational diabetes) and intrauterine programming of insulin resistance (IR). Maternal obesity (MO) and neonatal IR are associated with long-term development of obesity, diabetes mellitus, and increased global cardiovascular risk in the offspring. Multiple mechanisms of insulin signaling pathway impairment have been described in obese individuals, involving complex interactions of chronically elevated inflammatory mediators, adipokines, and the critical role of the endoplasmic reticulum (ER) stress-dependent unfolded protein response (UPR). However, the underlying cellular processes linking MO and IR in the offspring have not been fully elucidated. Here, we summarize the state-of-the-art evidence supporting the possibility that adverse metabolic postnatal outcomes such as IR in the offspring of pregnancies with MO and/or excessive GWG may be related to intrauterine activation of ER stress response.
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Obesity and excessive GWG are related to several maternal and fetal complications, including diabetes (pregestational and gestational diabetes) and intrauterine programming of insulin resistance (IR). Maternal obesity (MO) and neonatal IR are associated with long-term development of obesity, diabetes mellitus, and increased global cardiovascular risk in the offspring. Multiple mechanisms of insulin signaling pathway impairment have been described in obese individuals, involving complex interactions of chronically elevated inflammatory mediators, adipokines, and the critical role of the endoplasmic reticulum (ER) stress-dependent unfolded protein response (UPR). However, the underlying cellular processes linking MO and IR in the offspring have not been fully elucidated. 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subjects Apoptosis
Body mass index
Cardiovascular disease
Chronic illnesses
Colleges & universities
Complications and side effects
Development and progression
Diabetes
Diabetes, Gestational - genetics
Diabetes, Gestational - pathology
Endoplasmic reticulum
Endoplasmic Reticulum Stress - genetics
Female
Gynecology
Health aspects
Humans
Hypertension
Hypotheses
Infant, Newborn
Inflammation - genetics
Inflammation - pathology
Insulin - metabolism
Insulin resistance
Insulin Resistance - genetics
Laboratories
Medicine
Metabolism
Mortality
Obesity
Obesity - complications
Obesity - genetics
Obesity - pathology
Obstetrics
Pharmaceutical sciences
Physiology
Preeclampsia
Pregnancy
Pregnancy Complications - genetics
Pregnancy Complications - pathology
Pregnant women
Psychological aspects
Review
Risk factors
Stress response
title Programming of Fetal Insulin Resistance in Pregnancies with Maternal Obesity by ER Stress and Inflammation
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