Maternal and Postnatal Overnutrition Differentially Impact Appetite Regulators and Fuel Metabolism

  • Hui Chen
    Departments of Pharmacology (H.C., M.J.M.), School of Medical Sciences, University of New South Wales, New South Wales 2052, Australia
  • David Simar
    Health and Exercise Science (D.S.), School of Medical Sciences, University of New South Wales, New South Wales 2052, Australia
  • Karen Lambert
    Institut National de la Santé et de la Recherche Médicale ERI25 (K.L., J.M.), Muscle et Pathologies, Service de Physiologie Clinique, Centre Hospitalier Universitaire de Montpellier, 34295 Montpellier Cedex 5, France
  • Jacques Mercier
    Institut National de la Santé et de la Recherche Médicale ERI25 (K.L., J.M.), Muscle et Pathologies, Service de Physiologie Clinique, Centre Hospitalier Universitaire de Montpellier, 34295 Montpellier Cedex 5, France
  • Margaret J. Morris
    Departments of Pharmacology (H.C., M.J.M.), School of Medical Sciences, University of New South Wales, New South Wales 2052, Australia

説明

<jats:p>Maternal obesity is increasing, and it is known that the intrauterine experience programs fetal and newborn metabolism. However, the relative contributions of pre- or postnatal factors are unknown. We hypothesized that maternal overnutrition caused by long-term maternal obesity would exert a stronger detrimental impact than postnatal overnutrition on offspring metabolic homeostasis, with additional postnatal overnutrition exaggerating these alterations. Female Sprague Dawley rats were exposed to chow or high-fat cafeteria diet for 5 wk before mating and throughout gestation and lactation. On postnatal d 1, litters were adjusted to three per litter to induce postnatal overnutrition (vs. 12 in control). Hypothalamic appetite regulators neuropeptide Y and proopiomelanocortin, glucose transporter 4, and lipid metabolic markers were measured. At postnatal d 20, male pups born of obese dams, or those overnourished postnatally, were 42% heavier than controls; combining both interventions led to 80% greater body weight. Maternal obesity increased pup adiposity and led to glucose intolerance in offspring; these were exaggerated by additional postnatal overnutrition during lactation. Maternal obesity was also linked to hyperlipidemia in offspring and reduced hypothalamic neuropeptide Y and increased proopiomelanocortin mRNA expression. Postnatal overnutrition of offspring from obese dams amplified these hypothalamic changes. Both maternal and postnatal overnutrition reduced muscle glucose transporter 4. Adipose carnitine palmitoyl-transferase-1 and adipose triglyceride lipase mRNA was up-regulated only by postnatal overnutrition. Maternal overnutrition appears to alter central appetite circuits and promotes early-onset obesity; postnatal overnutrition interacted to cause peripheral lipid and glucose metabolic disorders, supporting the critical message to reduce early-life adverse nutritional impact.</jats:p>

収録刊行物

  • Endocrinology

    Endocrinology 149 (11), 5348-5356, 2008-07-17

    The Endocrine Society

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