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Carbohydrate Metabolism in Intrauterine Growth Retardation

  • Chapter
Metabolic Adaptation to Extrauterine Life

Part of the book series: Developments in Perinatal Medicine ((DIPM,volume 1))

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Abstract

Intrauterine growth retardation (IUGR) can result f m a variety of maternal, placental or fetal factors. Placental insufficiency (24, 25) and chronic vascular disease (36) are of major importance and result in diminution of uterine blood flow. The associated clinical picture is characterized by body wasting, the body weight being law for gestational age. Weight reduction of the organs is the result of diminished cell size (9, 42) and is most pronounced in the liver. The brain/body ratio is elevated because brain weight is relatively spared. The smallfor-gestational-age (SGA) infant is threatened by many hazards, one of which is the risk of neonatal hypoglycemia (11). Early glucose administration is, therefore, indicated (2, 11). Onset of hypoglycemia is mostly during the first day after delivery (23, 51). Exogenous glucose is cleared rapidly from the blood in these infants (30). It was accepted for many years that insufficient glycogen stores in SGA newborns could explain their increased risk of neonatal hypoglycemia. Several data, however, point to a more complex mechanism which has not been completely elucidated. The aim of this chapter is to review current knowledge on carbohydrate metabolism in IUGR in rat and man and to present some of our own data in the rat.

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Kollée, L.L.A., Monnens, L.A.H., Trijbels, J.M.F., Veerkamp, J.H. (1981). Carbohydrate Metabolism in Intrauterine Growth Retardation. In: De Meyer, R. (eds) Metabolic Adaptation to Extrauterine Life. Developments in Perinatal Medicine, vol 1. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-7514-2_8

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  • DOI: https://doi.org/10.1007/978-94-011-7514-2_8

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-011-7516-6

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