Abstract
It was demonstrated that hemolysed blood and/or crystalline hemoglobin inactivated insulin either by irreversible destruction due to the presence of SH compounds or by reversible binding to hemoglobin. The increased pancreatic insulin content and pancreatic islet cell hyperplasia observed in infants with erythroblastosis fetalis may represent a compensatory response to inactivation of circulating insulin.
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© 1967 by American Society of Hematology, Inc.
1967
