Time-restricted feeding reduces high-fat diet associated placental inflammation and limits adverse effects on fetal organ development.


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
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

415-421

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Auteurs

Aditya Upadhyay (A)

Dept. of Molecular Medicine & Biotechnology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India; Dr. A.P.J. Abdul Kalam Technical University Uttar Pradesh, Lucknow, India.

B Anjum (B)

Dept. of Molecular Medicine & Biotechnology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India; Dept of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.

Nachiket M Godbole (NM)

Dept. of Microbiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.

Sangam Rajak (S)

Dept of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.

Pooja Shukla (P)

Dept of Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.

Swasti Tiwari (S)

Dept. of Molecular Medicine & Biotechnology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.

Rohit A Sinha (RA)

Dept of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India. Electronic address: Anthony.rohit@gmail.com.

Madan M Godbole (MM)

Dept. of Molecular Medicine & Biotechnology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India. Electronic address: madangodbole@yahoo.co.in.

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