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Nutrients 2015, 7(2), 1202-1216; doi:10.3390/nu7021202

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.
Received: 24 December 2014 / Accepted: 2 February 2015 / Published: 12 February 2015
(This article belongs to the Special Issue Nutrition in Pregnancy)
View Full-Text   |   Download PDF [172 KB, uploaded 12 February 2015]

Abstract

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
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).

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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.

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