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    <title>Fennessey, P.V.</title>
    <link>http://repub.eur.nl/res/aut/8056/</link>
    <description>List of Publications</description>
    <language>en</language>
    <image>
      <url>http://repub.eur.nl/static-eur/img/logo.png</url>
      <title>RePub, Erasmus University Rotterdam</title>
      <link>http://repub.eur.nl</link>
    </image>
    <item>
      <title>Effect of dexamethasone on fetal hepatic glutamine-glutamate exchange (Article)</title>
      <link>http://repub.eur.nl/res/pub/9354/</link>
      <pubDate>2000-01-01T00:00:00Z</pubDate>
      <description>Intravenous infusion of dexamethasone (Dex) in the fetal lamb causes a
          two- to threefold increase in plasma glutamine and other glucogenic amino
          acids and a decrease of plasma glutamate to approximately one-third of
          normal. To explore the underlying mechanisms, hepatic amino acid uptake
          and conversion of L-[1-(13)C]glutamine to L-[1-(13)C]glutamate and
          (13)CO(2) were measured in six sheep fetuses before and in the last 2 h of
          a 26-h Dex infusion. Dex decreased hepatic glutamine and alanine uptakes
          (P &lt; 0.01) and hepatic glutamate output (P &lt; 0.001). Hepatic outputs of
          the glutamate (R(Glu,Gln)) and CO(2) formed from plasma glutamine
          decreased to 21 (P &lt; 0.001) and 53% (P = 0.009) of control, respectively.
          R(Glu,Gln), expressed as a fraction of both outputs, decreased (P &lt; 0.001)
          from 0.36 +/- 0.02 to 0.18 +/- 0.04. Hepatic glucose output remained
          virtually zero throughout the experiment. We conclude that Dex decreases
          fetal hepatic glutamate output by increasing the routing of glutamate
          carbon into the citric acid cycle and by decreasing the hepatic uptake of
          glucogenic amino acids.</description>
    </item> <item>
      <title>Relationship of fetal alanine uptake and placental alanine metabolism to maternal plasma alanine concentration (Article)</title>
      <link>http://repub.eur.nl/res/pub/8944/</link>
      <pubDate>1998-01-01T00:00:00Z</pubDate>
      <description>Uterine and umbilical uptakes of alanine (Ala) were measured in 10 ewes
          before (control) and during intravenous infusion of Ala, which increased
          maternal arterial Ala concentration from 115 +/- 14 to 629 +/- 78 microM
          (P &lt; 0.001). In 8 of these ewes, placental Ala fluxes were traced by
          constant intravenous infusion of L-[3,3,3-2H3]Ala in the mother and
          L-[1-13C]Ala in the fetus. Rates are reported as micromoles per minute per
          kilogram fetus. Ala infusion increased uterine uptake (2.5 +/- 0.6 to 15.6
          +/- 3.1, P &lt; 0.001), umbilical uptake (3.1 +/- 0.5 to 6.9 +/- 0.8, P &lt;
          0.001), and net uteroplacental utilization (-0.7 +/- 0.8 to 8.6 +/- 2.7, P
          &lt; 0.01) of Ala. Control Ala flux to fetus from mother (Rf,m) was much less
          than the Ala flux to fetus from placenta (Rf,p) (0.17 +/- 0.04 vs. 5. 0
          +/- 0.6). Two additional studies utilizing L-[U-13C]Ala as the maternal
          tracer confirmed the small relative contribution of Rf,m to Rf,p. During
          maternal Ala infusion, Rf,m increased significantly (P &lt; 0.02) but
          remained a small fraction of Rf,p (0.71 +/- 0.2 vs. 7.3 +/- 1.3). We
          conclude that maternal Ala entering the placenta is metabolized and
          exchanged for placental Ala, so that most of the Ala delivered to the
          fetus is produced within the placenta. An increase in maternal Ala
          concentration increases placental Ala utilization and the fetal uptake of
          both maternal and placental Ala.</description>
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