Sudden infant death and liver phosphoenolpyruvate carboxykinase analysis.
In an effort to substantiate the impaired gluconeogenesis-terminal hypoglycemia hypothesis of sudden infant death syndrome (SIDS), 52 infants ranging from 3 weeks to 7 months of age which had been brought to autopsy were studied. The stomach contents, vitreous humor glucose concentrations, hepatic glycogen content and hepatic phosphoenolpyruvate carboxykinase (PEPCK) activity were measured as part of the laboratory component of the postmortem investigation. The stomach contents, vitreous humor glucose concentrations and liver glycogen content were similar in SIDS/and non-SIDS victims. PEPCK activity was, however, significantly lower in SIDS (p < 0.001) victims and in SIDS with other findings (p < 0.01) victims when compared to non-SIDS victims. Despite the fact that SIDS victims had lower hepatic PEPCK activity and hence potentially lower gluconeogenic capacity, terminal hypoglycemia could not be demonstrated in this group as compared to the SIDS with other findings and the non-SIDS infants. The impaired gluconeogenesis-terminal hypoglycemia hypothesis thus could not be substantiated.
D000818:Animals; D005947:Glucose / Q000032:analysis; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008099:Liver / Q000201:enzymology*; D008112:Liver Glycogen / Q000032:analysis; D010729:Phosphoenolpyruvate Carboxykinase (GTP) / Q000032:analysis*; D051381:Rats; D013270:Stomach; D013398:Sudden Infant Death / Q000503:physiopathology*; D014822:Vitreous Body / Q000032:analysis
D008112:Liver Glycogen; D010729:Phosphoenolpyruvate Carboxykinase (GTP); D005947:Glucose