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Ketogenesis in Hypoglycemic Neonates
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Since hypoglycemic neonates do not exhibit compensative ketosis, we investigated the possible involvement of carnitine deficiency or Ω-oxidation in neonatal hypoglycemia. In a first group of 49 neonates, serum free fatty acid, acetoacetate and β-hydroxybutyrate concentrations were similar in hypoglycemic and normoglycemic neonates. Serum free carnitine concentrations did not show any difference in the hypoglycemic small-for-date infants (median 40 μmol/l, range 16–92 μmol/l) compared to the normoglycemic small-for-date infants (median 30 μmol/l, range 8–64 μmol/l). In a second group of 45 neonates, urinary excretion of dicarboxylic acids (adipic, suberic, sebaric and succinic acids) was similar in hypoglycemic infants compared to normoglycemic neonates. Despite the limitations of interpretaion of free carnitine determination, these data do not suggest an impaired β-oxidation by carnitine depletion or an enzymatic defect in hypoglycemic neonates.
Title: Ketogenesis in Hypoglycemic Neonates
Description:
Since hypoglycemic neonates do not exhibit compensative ketosis, we investigated the possible involvement of carnitine deficiency or Ω-oxidation in neonatal hypoglycemia.
In a first group of 49 neonates, serum free fatty acid, acetoacetate and β-hydroxybutyrate concentrations were similar in hypoglycemic and normoglycemic neonates.
Serum free carnitine concentrations did not show any difference in the hypoglycemic small-for-date infants (median 40 μmol/l, range 16–92 μmol/l) compared to the normoglycemic small-for-date infants (median 30 μmol/l, range 8–64 μmol/l).
In a second group of 45 neonates, urinary excretion of dicarboxylic acids (adipic, suberic, sebaric and succinic acids) was similar in hypoglycemic infants compared to normoglycemic neonates.
Despite the limitations of interpretaion of free carnitine determination, these data do not suggest an impaired β-oxidation by carnitine depletion or an enzymatic defect in hypoglycemic neonates.
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