Next Article in Journal
Novel Approaches to Improve the Intrinsic Microbiological Safety of Powdered Infant Milk Formula
Next Article in Special Issue
Association between Dietary Patterns during Pregnancy and Birth Size Measures in a Diverse Population in Southern US
Previous Article in Journal
Plant Ferritin—A Source of Iron to Prevent Its Deficiency
Previous Article in Special Issue
Sun Exposure and Vitamin D Supplementation in Relation to Vitamin D Status of Breastfeeding Mothers and Infants in the Global Exploration of Human Milk Study
Open AccessReview

Altered Fetal Skeletal Muscle Nutrient Metabolism Following an Adverse In Utero Environment and the Modulation of Later Life Insulin Sensitivity

1
Department of Physiology and Pharmacology, Western University, London, ON N6A-5C1, Canada
2
Department of Biology, Western University, London, ON N6A 5B7, Canada
3
Department of Obstetrics and Gynecology, Western University, London, ON N6H-5W9, Canada
4
Lawson Health Research Institute, London, ON N6C-2R5, Canada
5
Children's Health Research Institute, London, ON N6C-2V5, Canada
*
Author to whom correspondence should be addressed.
Nutrients 2015, 7(2), 1202-1216; https://doi.org/10.3390/nu7021202
Received: 24 December 2014 / Accepted: 2 February 2015 / Published: 12 February 2015
(This article belongs to the Special Issue Nutrition in Pregnancy)
The importance of the in utero environment as a contributor to later life metabolic disease has been demonstrated in both human and animal studies. In this review, we consider how disruption of normal fetal growth may impact skeletal muscle metabolic development, ultimately leading to insulin resistance and decreased insulin sensitivity, a key precursor to later life metabolic disease. In cases of intrauterine growth restriction (IUGR) associated with hypoxia, where the fetus fails to reach its full growth potential, low birth weight (LBW) is often the outcome, and early in postnatal life, LBW individuals display modifications in the insulin-signaling pathway, a critical precursor to insulin resistance. In this review, we will present literature detailing the classical development of insulin resistance in IUGR, but also discuss how this impaired development, when challenged with a postnatal Western diet, may potentially contribute to the development of later life insulin resistance. Considering the important role of the skeletal muscle in insulin resistance pathogenesis, understanding the in utero programmed origins of skeletal muscle deficiencies in insulin sensitivity and how they may interact with an adverse postnatal environment, is an important step in highlighting potential therapeutic options for LBW offspring born of pregnancies characterized by placental insufficiency. View Full-Text
Keywords: IUGR; hypoxia; obese; insulin sensitivity; skeletal muscle; mitochondria; β-oxidation; fats; acylcarnitine; oxygen IUGR; hypoxia; obese; insulin sensitivity; skeletal muscle; mitochondria; β-oxidation; fats; acylcarnitine; oxygen
MDPI and ACS Style

Dunlop, K.; Cedrone, M.; Staples, J.F.; Regnault, T.R. Altered Fetal Skeletal Muscle Nutrient Metabolism Following an Adverse In Utero Environment and the Modulation of Later Life Insulin Sensitivity. Nutrients 2015, 7, 1202-1216.

Show more citation formats Show less citations formats

Article Access Map by Country/Region

1
Only visits after 24 November 2015 are recorded.
Back to TopTop