Time-restricted feeding reduces high-fat diet associated placental inflammation and limits adverse effects on fetal organ development.
Apoptosis
/ drug effects
Autophagy
/ drug effects
Body Weight
/ drug effects
Diet, High-Fat
/ adverse effects
Endoplasmic Reticulum Stress
/ drug effects
Fasting
Female
Fetus
/ drug effects
Humans
Inflammation
/ prevention & control
Metabolic Diseases
/ prevention & control
Obesity
/ blood
Oxidative Stress
/ drug effects
Placenta
/ drug effects
Pregnancy
Prenatal Exposure Delayed Effects
/ prevention & control
Triglycerides
/ blood
Autophagy
Hepatosteatosis
Inflammation
Obesity
Oxidative stress
Placenta
Time-restricted feeding
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
25 06 2019
25 06 2019
Historique:
received:
15
04
2019
accepted:
22
04
2019
pubmed:
6
5
2019
medline:
7
7
2020
entrez:
5
5
2019
Statut:
ppublish
Résumé
Maternal nutrition has become a major public health concern over recent years and is a known predictor of adverse long-term metabolic derangement in offspring. Time-restricted feeding (TRF), wherein food consumption is restricted to the metabolically active phase of the day, is a dietary approach that improves metabolic parameters when consuming a high-fat diet (HFD). Here, we tested whether TRF could reduce maternal HFD associated inflammation and thereby mitigate defects in fetal organ developmental. Female rats were kept on following three dietary regimens; Ad libitum normal chow diet (NCD-AL), Ad libitum HFD (HFD-AL) and Time-restricted fed HFD (HFD-TRF) from 5 months prior to mating and continued throughout pregnancy. Rat dams were sacrificed at embryonic day 18.5 (ED18.5) and placental tissues from these rats were processed for the analysis of cellular apoptosis, inflammatory cytokines (TNFα and IL-6), oxidative stress, endoplasmic reticulum (ER) stress and autophagy. Furthermore, fetal hepatic triglyceride (TG) content and fetal lung maturation were assessed at ED18.5. Biochemical analysis revealed that HFD-TRF rat had significantly lower serum TG levels and body weight compared to HFD-AL rats. Additionally, TRF significantly blocked HFD-induced placental apoptosis and inflammation via minimizing cellular stress, and restoring autophagic flux. In addition, fetal hepatosteatosis and delayed fetal lung maturation induced by HFD was significantly ameliorated in HFD-TRF compared to HFD-AL. Collectively, our results suggest that reducing placental inflammation via TRF could prevent adverse fetal metabolic outcomes in pregnancies complicated by maternal obesity.
Identifiants
pubmed: 31053302
pii: S0006-291X(19)30805-8
doi: 10.1016/j.bbrc.2019.04.154
pii:
doi:
Substances chimiques
Triglycerides
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
415-421Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.