Placental mTOR Signaling and Sexual Dimorphism in Metabolic Health across the Lifespan of Offspring

Robust evidence of fetal programming of adult disease has surfaced in the last several decades. Human and preclinical investigations of intrauterine insults report perturbations in placental nutrient sensing by the mechanistic target of rapamycin (mTOR). This review focuses on pregnancy complication...

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Autores principales:	Megan Beetch, Emilyn U. Alejandro
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	mTOR signaling placenta pregnancy fetal growth restriction birth weight obesity Pediatrics RJ1-570
Acceso en línea:	https://doaj.org/article/8c198d0bb2b54951a6a56c50b8475bc9
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spelling	oai:doaj.org-article:8c198d0bb2b54951a6a56c50b8475bc92021-11-25T17:14:03ZPlacental mTOR Signaling and Sexual Dimorphism in Metabolic Health across the Lifespan of Offspring10.3390/children81109702227-9067https://doaj.org/article/8c198d0bb2b54951a6a56c50b8475bc92021-10-01T00:00:00Zhttps://www.mdpi.com/2227-9067/8/11/970https://doaj.org/toc/2227-9067Robust evidence of fetal programming of adult disease has surfaced in the last several decades. Human and preclinical investigations of intrauterine insults report perturbations in placental nutrient sensing by the mechanistic target of rapamycin (mTOR). This review focuses on pregnancy complications associated with placental mTOR regulation, such as fetal growth restriction (FGR), fetal overgrowth, gestational diabetes mellitus (GDM), polycystic ovarian syndrome (PCOS), maternal nutrient restriction (MNR), preeclampsia (PE), maternal smoking, and related effects on offspring birthweight. The link between mTOR-associated birthweight outcomes and offspring metabolic health trajectory with a focus on sexual dimorphism are discussed. Both human physiology and animal models are summarized to facilitate in depth understanding. GDM, PCOS and fetal overgrowth are associated with increased placental mTOR, whereas FGR, MNR and maternal smoking are linked to decreased placental mTOR activity. Generally, birth weight is reduced in complications with decreased mTOR (i.e., FGR, MNR, maternal smoking) and higher with increased mTOR (GDM, PCOS). Offspring display obesity or a higher body mass index in childhood and adulthood, impaired glucose and insulin tolerance in adulthood, and deficiencies in pancreatic beta-cell mass and function compared to offspring from uncomplicated pregnancies. Defining causal players in the fetal programming of offspring metabolic health across the lifespan will aid in stopping the vicious cycle of obesity and type II diabetes.Megan BeetchEmilyn U. AlejandroMDPI AGarticlemTOR signalingplacentapregnancyfetal growth restrictionbirth weightobesityPediatricsRJ1-570ENChildren, Vol 8, Iss 970, p 970 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	mTOR signaling placenta pregnancy fetal growth restriction birth weight obesity Pediatrics RJ1-570
spellingShingle	mTOR signaling placenta pregnancy fetal growth restriction birth weight obesity Pediatrics RJ1-570 Megan Beetch Emilyn U. Alejandro Placental mTOR Signaling and Sexual Dimorphism in Metabolic Health across the Lifespan of Offspring
description	Robust evidence of fetal programming of adult disease has surfaced in the last several decades. Human and preclinical investigations of intrauterine insults report perturbations in placental nutrient sensing by the mechanistic target of rapamycin (mTOR). This review focuses on pregnancy complications associated with placental mTOR regulation, such as fetal growth restriction (FGR), fetal overgrowth, gestational diabetes mellitus (GDM), polycystic ovarian syndrome (PCOS), maternal nutrient restriction (MNR), preeclampsia (PE), maternal smoking, and related effects on offspring birthweight. The link between mTOR-associated birthweight outcomes and offspring metabolic health trajectory with a focus on sexual dimorphism are discussed. Both human physiology and animal models are summarized to facilitate in depth understanding. GDM, PCOS and fetal overgrowth are associated with increased placental mTOR, whereas FGR, MNR and maternal smoking are linked to decreased placental mTOR activity. Generally, birth weight is reduced in complications with decreased mTOR (i.e., FGR, MNR, maternal smoking) and higher with increased mTOR (GDM, PCOS). Offspring display obesity or a higher body mass index in childhood and adulthood, impaired glucose and insulin tolerance in adulthood, and deficiencies in pancreatic beta-cell mass and function compared to offspring from uncomplicated pregnancies. Defining causal players in the fetal programming of offspring metabolic health across the lifespan will aid in stopping the vicious cycle of obesity and type II diabetes.
format	article
author	Megan Beetch Emilyn U. Alejandro
author_facet	Megan Beetch Emilyn U. Alejandro
author_sort	Megan Beetch
title	Placental mTOR Signaling and Sexual Dimorphism in Metabolic Health across the Lifespan of Offspring
title_short	Placental mTOR Signaling and Sexual Dimorphism in Metabolic Health across the Lifespan of Offspring
title_full	Placental mTOR Signaling and Sexual Dimorphism in Metabolic Health across the Lifespan of Offspring
title_fullStr	Placental mTOR Signaling and Sexual Dimorphism in Metabolic Health across the Lifespan of Offspring
title_full_unstemmed	Placental mTOR Signaling and Sexual Dimorphism in Metabolic Health across the Lifespan of Offspring
title_sort	placental mtor signaling and sexual dimorphism in metabolic health across the lifespan of offspring
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/8c198d0bb2b54951a6a56c50b8475bc9
work_keys_str_mv	AT meganbeetch placentalmtorsignalingandsexualdimorphisminmetabolichealthacrossthelifespanofoffspring AT emilynualejandro placentalmtorsignalingandsexualdimorphisminmetabolichealthacrossthelifespanofoffspring
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Placental mTOR Signaling and Sexual Dimorphism in Metabolic Health across the Lifespan of Offspring

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