Maternal and Postnatal Overnutrition Differentially Impact Appetite Regulators and Fuel Metabolism
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- Hui Chen
- Departments of Pharmacology (H.C., M.J.M.), School of Medical Sciences, University of New South Wales, New South Wales 2052, Australia
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- David Simar
- Health and Exercise Science (D.S.), School of Medical Sciences, University of New South Wales, New South Wales 2052, Australia
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- 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
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- 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
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- 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
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- Endocrinology
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Endocrinology 149 (11), 5348-5356, 2008-07-17
The Endocrine Society