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Red cell glycolytic intermediates in normal, anaemic and transfused human fetuses
Author(s) -
Lestas A. N.,
Bellingham A. J.,
Nicolaides K. H.
Publication year - 1989
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1989.tb07758.x
Subject(s) - reticulocytosis , glycolysis , fetus , hexokinase , red cell , medicine , endocrinology , phosphofructokinase , biology , pyruvate kinase , fructose , biochemistry , metabolism , pregnancy , anemia , genetics
Summary Normal fetal ranges for red cell glycolytic intermediates at 18–24 weeks gestation, which are useful as reference values for the prenatal diagnosis of erythroenzymopathies, were established for the first time. Characteristic increases in glucose‐6‐phosphate (G6P), fructose‐6‐phosphate (F6P) and particularly fructose‐ 1,6‐diphosphate (FDP) suggest that there is no metabolic block at the phospho‐fructokinase (PFK) step of glycolysis as previously suggested by others for premature infants on the first day of life. Neither reticulocytosis nor anaemia consistently led to further increases in the early metabolites as occurs in adults. However, very large increases in G6P, F6P and particularly FDP may occur independently of anaemia and reticulocytosis. This suggests that activation of hexokinase (HK) and/or PFK can take place as in adults but the stimulus is probably different to adults. The 2,3‐DPG in normal fetuses is higher than in adults and increases still further in anaemic fetuses with or without transfusion of adult blood. The pattern of intermediates found in the fetus suggests that the controlling mechanism for the increased 2,3‐DPG may be an in vivo relative preponderance of PFK activity over that of pyruvate kinase (PK) rather than regulation of HK as proposed for adult subjects with anaemia or high altitude hypoxia.