Developmental programming of metabolic syndrome in individuals born with intrauterine growth restriction followed by accelerated postnatal catch-up growth: exploration of outcomes in adulthood
Détails
Télécharger: Mémoire no 4391 M. Keshavjee.pdf (1494.26 [Ko])
Etat: Public
Version: Après imprimatur
Licence: Non spécifiée
Etat: Public
Version: Après imprimatur
Licence: Non spécifiée
ID Serval
serval:BIB_410865495460
Type
Mémoire
Sous-type
(Mémoire de) maîtrise (master)
Collection
Publications
Institution
Titre
Developmental programming of metabolic syndrome in individuals born with intrauterine growth restriction followed by accelerated postnatal catch-up growth: exploration of outcomes in adulthood
Directeur⸱rice⸱s
SIMEONI U.
Codirecteur⸱rice⸱s
YZYDORCZYK C.
Détails de l'institution
Université de Lausanne, Faculté de biologie et médecine
Statut éditorial
Acceptée
Date de publication
2017
Langue
anglais
Nombre de pages
23
Résumé
INTRODUCTION
The hypothesis that some noncommunicable diseases may find important parts of their origins early in life is currently known as Developmental programming or Developmental origins of health and disease (DOHaD). Several epidemiological studies have reported that intrauterine growth restriction (IUGR) increases the susceptibility to develop diabetes, obesity and associated disturbances later in life. The risk might even be amplified if a postnatal catch-up growth follows IUGR. The aim of this study is to evaluate in adult rats several metabolic alterations induced by IUGR followed by postnatal catch-up growth in both gender, in order to, thereafter, identify the potentially involved mechanisms.
METHODS
An IUGR rat model was obtained by maternal exposure to a low protein diet (9% casein) throughout the gestation compared to a control diet (23% casein). At birth, litter size was adjusted to 10 or reduced to 4 pups (2 males and 2 females) per mother inducing a transient postnatal overfeeding (OF) and catch-up growth due to the surplus of milk availability for each offspring. Body weight measurement, computed tomography adipose tissue quantification, glucose tolerance tests, liver histology and plasma analyses were performed.
RESULTS
Higher visceral fat content, altered tolerance to glucose, hepatic steatosis and fibrosis, increased plasma levels of cholesterol, triglycerides and transaminases were retrieved in male and female rats with either IUGR, postnatal catch-up growth or both IUGR and subsequent postnatal catch-up growth between 6 and 12 months of age compared to controls.
CONCLUSION
IUGR and accelerated postnatal catch-up growth generate lifelong consequences with adverse metabolic outcomes thereafter. Indeed, several metabolic syndrome components were retrieved in adulthood. Therefore, exploring the developmental programming involved mechanisms and finding biomarkers to identify individuals at risk may provide opportunities for lifestyle interventions and disease prevention, especially during the current diabetes and obesity pandemic.
The hypothesis that some noncommunicable diseases may find important parts of their origins early in life is currently known as Developmental programming or Developmental origins of health and disease (DOHaD). Several epidemiological studies have reported that intrauterine growth restriction (IUGR) increases the susceptibility to develop diabetes, obesity and associated disturbances later in life. The risk might even be amplified if a postnatal catch-up growth follows IUGR. The aim of this study is to evaluate in adult rats several metabolic alterations induced by IUGR followed by postnatal catch-up growth in both gender, in order to, thereafter, identify the potentially involved mechanisms.
METHODS
An IUGR rat model was obtained by maternal exposure to a low protein diet (9% casein) throughout the gestation compared to a control diet (23% casein). At birth, litter size was adjusted to 10 or reduced to 4 pups (2 males and 2 females) per mother inducing a transient postnatal overfeeding (OF) and catch-up growth due to the surplus of milk availability for each offspring. Body weight measurement, computed tomography adipose tissue quantification, glucose tolerance tests, liver histology and plasma analyses were performed.
RESULTS
Higher visceral fat content, altered tolerance to glucose, hepatic steatosis and fibrosis, increased plasma levels of cholesterol, triglycerides and transaminases were retrieved in male and female rats with either IUGR, postnatal catch-up growth or both IUGR and subsequent postnatal catch-up growth between 6 and 12 months of age compared to controls.
CONCLUSION
IUGR and accelerated postnatal catch-up growth generate lifelong consequences with adverse metabolic outcomes thereafter. Indeed, several metabolic syndrome components were retrieved in adulthood. Therefore, exploring the developmental programming involved mechanisms and finding biomarkers to identify individuals at risk may provide opportunities for lifestyle interventions and disease prevention, especially during the current diabetes and obesity pandemic.
Mots-clé
Developmental programming, developmental origins of health and disease, metabolic syndrome, intrauterine growth restriction, postnatal catch-up growth
Création de la notice
05/09/2018 10:07
Dernière modification de la notice
08/09/2020 6:08