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Maternal protein restriction during lactation induces early and lasting plasma metabolomic and hepatic lipidomic signatures of the offspring in a rodent programming model.
J Nutr Biochem 2018; 55:124-141JN

Abstract

Perinatal undernutrition affects not only fetal and neonatal growth but also adult health outcome, as suggested by the metabolic imprinting concept. However, the exact mechanisms underlying offspring metabolic adaptations are not yet fully understood. Specifically, it remains unclear whether the gestation or the lactation is the more vulnerable period to modify offspring metabolic flexibility. We investigated in a rodent model of intrauterine growth restriction (IUGR) induced by maternal protein restriction (R) during gestation which time window of maternal undernutrition (gestation, lactation or gestation-lactation) has more impact on the male offspring metabolomics phenotype. Plasma metabolome and hepatic lipidome of offspring were characterized through suckling period and at adulthood using liquid chromatography-high-resolution mass spectrometry. Multivariate analysis of these fingerprints highlighted a persistent metabolomics signature in rats suckled by R dams, with a clear-cut discrimination from offspring fed by control (C) dams. Pups submitted to a nutritional switch at birth presented a metabolomics signature clearly distinct from that of pups nursed by dams maintained on a consistent perinatal diet. Control rats suckled by R dams presented transiently higher branched-chain amino acid (BCAA) oxidation during lactation besides increased fatty acid (FA) β-oxidation, associated with preserved insulin sensitivity and lesser fat accretion that persisted throughout their life. In contrast, IUGR rats displayed permanently impaired β-oxidation, associated to increased glucose or BCAA oxidation at adulthood, depending on the fact that pups experienced slow postnatal or catch-up growth, as suckled by R or C dams, respectively. Taken together, these findings provide evidence for a significant contribution of the lactation period in metabolic programming.

Authors+Show Affiliations

INRA, UMR1280, Physiopathologie des Adaptations Nutritionnelles, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France; LUNAM, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France.Nantes University, House of the Human Sciences-USR3491, Nantes, F-44021, France.INRA, UMR1280, Physiopathologie des Adaptations Nutritionnelles, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France; LUNAM, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France.INRA, UMR1280, Physiopathologie des Adaptations Nutritionnelles, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France; LUNAM, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France.INRA, UMR1280, Physiopathologie des Adaptations Nutritionnelles, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France; LUNAM, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France.LUNAM University, Angers, France; INSERM U1063, Angers, France.INRA, UMR1280, Physiopathologie des Adaptations Nutritionnelles, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France; LUNAM, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France.StatSC, ONIRIS, INRA, 44322, Nantes, France.INRA, UMR1280, Physiopathologie des Adaptations Nutritionnelles, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France; Nantes University Hospital, France.LUNAM, Oniris, Laboratoire d'Etude des Résidus et Contaminants dans les Aliments (LABERCA), USC INRA 1329, Nantes, France.INRA, UMR1280, Physiopathologie des Adaptations Nutritionnelles, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France; LUNAM, Institut des maladies de l'appareil digestif (IMAD), Centre de Recherche en Nutrition Humaine Ouest (CRNH), Nantes, France. Electronic address: Marie-Cecile.Alexandre-Gouabau@univ-nantes.fr.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29413487

Citation

Martin Agnoux, Aurore, et al. "Maternal Protein Restriction During Lactation Induces Early and Lasting Plasma Metabolomic and Hepatic Lipidomic Signatures of the Offspring in a Rodent Programming Model." The Journal of Nutritional Biochemistry, vol. 55, 2018, pp. 124-141.
Martin Agnoux A, El Ghaziri A, Moyon T, et al. Maternal protein restriction during lactation induces early and lasting plasma metabolomic and hepatic lipidomic signatures of the offspring in a rodent programming model. J Nutr Biochem. 2018;55:124-141.
Martin Agnoux, A., El Ghaziri, A., Moyon, T., Pagniez, A., David, A., Simard, G., ... Alexandre-Gouabau, M. C. (2018). Maternal protein restriction during lactation induces early and lasting plasma metabolomic and hepatic lipidomic signatures of the offspring in a rodent programming model. The Journal of Nutritional Biochemistry, 55, pp. 124-141. doi:10.1016/j.jnutbio.2017.11.009.
Martin Agnoux A, et al. Maternal Protein Restriction During Lactation Induces Early and Lasting Plasma Metabolomic and Hepatic Lipidomic Signatures of the Offspring in a Rodent Programming Model. J Nutr Biochem. 2018;55:124-141. PubMed PMID: 29413487.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Maternal protein restriction during lactation induces early and lasting plasma metabolomic and hepatic lipidomic signatures of the offspring in a rodent programming model. AU - Martin Agnoux,Aurore, AU - El Ghaziri,Angélina, AU - Moyon,Thomas, AU - Pagniez,Anthony, AU - David,Agnès, AU - Simard,Gilles, AU - Parnet,Patricia, AU - Qannari,El Mostafa, AU - Darmaun,Dominique, AU - Antignac,Jean-Philippe, AU - Alexandre-Gouabau,Marie-Cécile, Y1 - 2017/12/10/ PY - 2017/05/19/received PY - 2017/10/12/revised PY - 2017/11/14/accepted PY - 2018/2/8/pubmed PY - 2018/2/8/medline PY - 2018/2/8/entrez KW - Energy homeostasis KW - Lactation KW - Metabolic programming KW - Metabolomics and lipidomics profiles KW - Perinatal maternal protein restriction SP - 124 EP - 141 JF - The Journal of nutritional biochemistry JO - J. Nutr. Biochem. VL - 55 N2 - Perinatal undernutrition affects not only fetal and neonatal growth but also adult health outcome, as suggested by the metabolic imprinting concept. However, the exact mechanisms underlying offspring metabolic adaptations are not yet fully understood. Specifically, it remains unclear whether the gestation or the lactation is the more vulnerable period to modify offspring metabolic flexibility. We investigated in a rodent model of intrauterine growth restriction (IUGR) induced by maternal protein restriction (R) during gestation which time window of maternal undernutrition (gestation, lactation or gestation-lactation) has more impact on the male offspring metabolomics phenotype. Plasma metabolome and hepatic lipidome of offspring were characterized through suckling period and at adulthood using liquid chromatography-high-resolution mass spectrometry. Multivariate analysis of these fingerprints highlighted a persistent metabolomics signature in rats suckled by R dams, with a clear-cut discrimination from offspring fed by control (C) dams. Pups submitted to a nutritional switch at birth presented a metabolomics signature clearly distinct from that of pups nursed by dams maintained on a consistent perinatal diet. Control rats suckled by R dams presented transiently higher branched-chain amino acid (BCAA) oxidation during lactation besides increased fatty acid (FA) β-oxidation, associated with preserved insulin sensitivity and lesser fat accretion that persisted throughout their life. In contrast, IUGR rats displayed permanently impaired β-oxidation, associated to increased glucose or BCAA oxidation at adulthood, depending on the fact that pups experienced slow postnatal or catch-up growth, as suckled by R or C dams, respectively. Taken together, these findings provide evidence for a significant contribution of the lactation period in metabolic programming. SN - 1873-4847 UR - https://www.unboundmedicine.com/medline/citation/29413487/Maternal_protein_restriction_during_lactation_induces_early_and_lasting_plasma_metabolomic_and_hepatic_lipidomic_signatures_of_the_offspring_in_a_rodent_programming_model_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0955-2863(17)30434-5 DB - PRIME DP - Unbound Medicine ER -