title: Long-term impact of an antioxidant-deficient neonatal diet on lipid and glucose metabolism.
abstract: Newborn infants are at risk for oxidative stress leading to metabolic syndrome features. Oxidative stress can be induced by oxidant load such as oxygen supplementation, peroxides from intravenous nutrition, or low antioxidant defenses. We hypothesize that a modulation of antioxidant defenses during the neonatal period, without external oxidant challenge, will have a long-term influence on energy metabolism. Guinea pigs were fed between their third and their seventh day of life a regular chow leading to "mature" antioxidant defenses or a deficient chow leading to lower antioxidant defenses. Between weeks 1 and 14, the animals were fed regular chow. The hepatic oxidized redox status of glutathione associated with the deficient diet (-221 +/- 2 vs -228 +/- 1 mV, p < 0.01) was maintained until 14 weeks. At 13-14 weeks, animals fed the deficient diet presented lower plasma TG (479 +/- 57 vs 853 +/- 32 microM, p < 0.01), lower blood glucose (5.8 +/- 0.3 vs 6.9 +/- 0.3 mM, p < 0.05), and better tolerance to glucose (p < 0.05). Blood glucose correlated negatively with the redox status (r2 = 0.47, p < 0.01). Low antioxidant defenses during the neonatal period induce a better energy substrate profile associated with an oxidized redox status later in life. These findings suggest being aware of negative consequences when adopting "aggressive" antioxidant therapies in newborn infants.
authors.affiliation: Department of Nutrition, CHU Sainte-Justine, Faculty of Medicine, University of Montréal, Montréal, QC, Canada H3T 1C5.
authors.forename: Valérie
authors.initials: V
authors.lastname: Turcot
authors.forename: Thérèse
authors.initials: T
authors.lastname: Rouleau
authors.forename: Apollinaire
authors.initials: A
authors.lastname: Tsopmo
authors.forename: Nathalie
authors.initials: N
authors.lastname: Germain
authors.forename: Léna
authors.initials: L
authors.lastname: Potvin
authors.forename: Anne-Monique
authors.initials: AM
authors.lastname: Nuyt
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Lavoie
mesh_terms: D000103:Acetyl-CoA Carboxylase / Q000235:genetics / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D000975:Antioxidants / Q000378:metabolism; D004035:Diet Therapy / Q000639:trends; D015237:Dinoprost / Q000031:analogs & derivatives / Q000378:metabolism; D005526:Food, Formulated; D018507:Gene Expression Regulation, Developmental; D005947:Glucose / Q000378:metabolism*; D005951:Glucose Tolerance Test; D005978:Glutathione / Q000378:metabolism; D006168:Guinea Pigs; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics / Q000378:metabolism; D050356:Lipid Metabolism; D008099:Liver / Q000502:physiology*; D024821:Metabolic Syndrome / Q000097:blood / Q000178:diet therapy / Q000235:genetics / Q000378:metabolism*; D010084:Oxidation-Reduction; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D000975:Antioxidants; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D014280:Triglycerides; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost; D013482:Superoxide Dismutase; D000103:Acetyl-CoA Carboxylase; D005978:Glutathione; D005947:Glucose