The influence of maternal protein nutrition on offspring development and metabolism: the role of glucocorticoids

• Published in: Proceedings of the Nutrition Society 2012-02, Vol.71 (1), p.198-203
• Main Authors: Almond, K., Bikker, P., Lomax, M., Symonds, M. E., Mostyn, A.
• Format: Article
• Language: English
• Subjects: Animals; Birth weight; Body weight; Dehydrogenases; Diet; Dietary Proteins - pharmacology; Dietary Supplements; Digestive system; Disease; Female; Fetal Development - drug effects; Fetal Development - physiology; Fetuses; Glucocorticoids - metabolism; Hormones; Human subjects; Hydroxysteroid Dehydrogenases - metabolism; Hypertension; Liver - metabolism; Malnutrition; Metabolic Diseases - etiology; Metabolic disorders; Nutrition; Offspring; Postgraduate Symposium; Pregnancy; Pregnancy Complications; Prenatal Exposure Delayed Effects; Prenatal Nutritional Physiological Phenomena; Protein-Energy Malnutrition - complications; Proteins; Receptors, Glucocorticoid - metabolism; Sheep; Swine; Up-Regulation
• ISSN: 0029-6651; 1475-2719
• DOI: 10.1017/S0029665111003363

The consequences of sub-optimal nutrition through alterations in the macronutrient content of the maternal diet will not simply be reflected in altered neonatal body composition and increased mortality, but are likely to continue into adulthood and confer greater risk of metabolic disease. One mechanism linking manipulations of the maternal environment to an increased risk of later disease is enhanced fetal exposure to glucocorticoids (GC). Tissue sensitivity to cortisol is regulated, in part, by the GC receptor and 11β-hydroxysteroid dehydrogenase (11β-HSD) types 1 and 2. Several studies have shown the effects of maternal undernutrition, particularly low-protein diets, on the programming of GC action in the offspring; however, dietary excess is far more characteristic of the diets consumed by contemporary pregnant women. This study investigated the programming effects of moderate protein supplementation in pigs throughout pregnancy. We have demonstrated an up-regulation of genes involved in GC sensitivity, such as GC receptor and 11β-HSD, in the liver, but have yet to detect any other significant changes in these piglets, with no differences observed in body weight or composition. This increase in GC sensitivity was similar to the programming effects observed following maternal protein restriction or global undernutrition during pregnancy.