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Susan Gray Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
Department of Pediatrics, Brown University Medical School and Women and Infants’ Hospital of Rhode Island, Providence, Rhode Island 02912, USA
Department of Pediatrics, University of Pittsburgh School of Medicine and Magee-Womens Research Institute, Pittsburgh, Pennsylvania 15261, USA

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Barbara S Stonestreet Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
Department of Pediatrics, Brown University Medical School and Women and Infants’ Hospital of Rhode Island, Providence, Rhode Island 02912, USA
Department of Pediatrics, University of Pittsburgh School of Medicine and Magee-Womens Research Institute, Pittsburgh, Pennsylvania 15261, USA

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Shanthie Thamotharan Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
Department of Pediatrics, Brown University Medical School and Women and Infants’ Hospital of Rhode Island, Providence, Rhode Island 02912, USA
Department of Pediatrics, University of Pittsburgh School of Medicine and Magee-Womens Research Institute, Pittsburgh, Pennsylvania 15261, USA

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Grazyna B Sadowska Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
Department of Pediatrics, Brown University Medical School and Women and Infants’ Hospital of Rhode Island, Providence, Rhode Island 02912, USA
Department of Pediatrics, University of Pittsburgh School of Medicine and Magee-Womens Research Institute, Pittsburgh, Pennsylvania 15261, USA

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Molly Daood Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
Department of Pediatrics, Brown University Medical School and Women and Infants’ Hospital of Rhode Island, Providence, Rhode Island 02912, USA
Department of Pediatrics, University of Pittsburgh School of Medicine and Magee-Womens Research Institute, Pittsburgh, Pennsylvania 15261, USA

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Jon Watchko Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
Department of Pediatrics, Brown University Medical School and Women and Infants’ Hospital of Rhode Island, Providence, Rhode Island 02912, USA
Department of Pediatrics, University of Pittsburgh School of Medicine and Magee-Womens Research Institute, Pittsburgh, Pennsylvania 15261, USA

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Sherin U Devaskar Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
Department of Pediatrics, Brown University Medical School and Women and Infants’ Hospital of Rhode Island, Providence, Rhode Island 02912, USA
Department of Pediatrics, University of Pittsburgh School of Medicine and Magee-Womens Research Institute, Pittsburgh, Pennsylvania 15261, USA

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We investigated the effects of maternal antenatal dexamethasone (Dex) treatment given as a single course (4 doses) or multiple courses (20 doses) on fetal skeletal muscle glucose transporter (GLUT) protein concentrations at 70% of gestation (106 to 107 days with term being 145 to 150 days) in the ovine fetus. Antenatal corticosteroid administration was associated with a decrease in endogenous fetal plasma cortisol concentrations (P < 0.05), fetal hyperglycemia (P < 0.02) and hyperinsulinemia (P < 0.05). These metabolic/hormonal changes were associated with a decrease in fetal body weight (P < 0.05) in the multiple course Dex group compared with the multiple course placebo group. These perturbations were associated with an increase in fetal skeletal muscle GLUT 1 concentrations that mediate basal glucose transport in the extensor digitorum lateralis and extensor digitorum longus muscles (P < 0.05) 18 h after the last dose of Dex was given in the single course group. However, in the multiple course Dex group, a small increase in GLUT 1 was observed only in the biceps femoris. In contrast, both single and multiple courses of antenatal Dex were associated with an increase in the extensor digitorum lateralis and biceps femoris muscle GLUT 4 (insulin-responsive) concentrations (P < 0.05). We conclude that antenatal corticosteroids perturb fetal glucose/insulin homeostasis, which is associated with increases in fetal skeletal muscle glucose transporters to compensate for and attenuate the associated catabolic fetal state. These changes consist of an increase in proteins that mediate basal glucose transport (GLUT 1) to meet immediate energy requirements of the fetal skeletal muscle with an increase in basal insulin sensitivity (GLUT 4) to compensate for the Dex-induced catabolic state after exposure to multiple courses of Dex.

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