Next Article in Journal
Bevacizumab-Based Chemotherapy Combined with Regional Deep Capacitive Hyperthermia in Metastatic Cancer Patients: A Pilot Study
Next Article in Special Issue
Gut–CNS-Axis as Possibility to Modulate Inflammatory Disease Activity—Implications for Multiple Sclerosis
Previous Article in Journal
Role of Hormones in the Regulation of RACK1 Expression as a Signaling Checkpoint in Immunosenescence
Previous Article in Special Issue
Ontogeny of Sex-Related Differences in Foetal Developmental Features, Lipid Availability and Fatty Acid Composition
Article Menu
Issue 7 (July) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2017, 18(7), 1451; doi:10.3390/ijms18071451

Maternal Macronutrient Consumption and the Developmental Origins of Metabolic Disease in the Offspring

1
Department of Pharmacology & Therapeutics, University of Manitoba, Winnipeg, MB R3E 3P4, Canada
2
Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Research Theme of the Children’s Hospital Research Institute of Manitoba, University of Manitoba, Winnipeg, MB R3E 3P4, Canada
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 8 March 2017 / Revised: 14 June 2017 / Accepted: 30 June 2017 / Published: 6 July 2017
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
View Full-Text   |   Download PDF [300 KB, uploaded 6 July 2017]   |  

Abstract

Recent research aimed at understanding the rise in obesity and cardiometabolic disease in children suggests that suboptimal maternal nutrition conditions organ systems and physiological responses in the offspring contributing to disease development. Understanding the mechanisms by which the macronutrient composition of the maternal diet during pregnancy or lactation affects health outcomes in the offspring may lead to new maternal nutrition recommendations, disease prevention strategies and therapies that reduce the increasing incidence of cardiometabolic disease in children. Recent mechanistic animal model research has identified how excess fats and sugars in the maternal diet alter offspring glucose tolerance, insulin signaling and metabolism. Maternal nutrition appears to influence epigenetic alterations in the offspring and the programming of gene expression in key metabolic pathways. This review is focused on experimental studies in animal models that have investigated mechanisms of how maternal consumption of macronutrients affects cardiometabolic disease development in the offspring. Future research using “-omic” technologies is essential to elucidate the mechanisms of how altered maternal macronutrient consumption influences the development of disease in the offspring. View Full-Text
Keywords: developmental programming; metabolic disease; cardiovascular disease; high-fat diet; sucrose developmental programming; metabolic disease; cardiovascular disease; high-fat diet; sucrose
Figures

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Kereliuk, S.M.; Brawerman, G.M.; Dolinsky, V.W. Maternal Macronutrient Consumption and the Developmental Origins of Metabolic Disease in the Offspring. Int. J. Mol. Sci. 2017, 18, 1451.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top