Abstract
Cause and effect are implied in the term ‘ketotic jhypoglycemia’ used by COLLE and ULSTROM (J. Ped. 64: 632 [1964]) to describe a childhood syndrome of hypoglycemic convulsions associated with ketonuria. MADISON (J.clin. Invest. 43: 408 [1963]) showed a stimulatory effect of ketones on insulin secretion and postulated this as a feedback mechanism to prevent fatal ketosis. Two techniques to induce ketosis were used to study patients with ketotic hypoglycemia: 1. β-OHB was infused intravenously during a 2 to 6 hour period; 2. Heparin was injected intramuscularly to promote lipolysis. Patients fasted throughout the test period. The response of patients and control subjects was compared to a control day when no heparin was given. Blood sugar (BS), immunoreactive insulin (IRI), non-esterified fatty acids (NEFA) and ketones were measured. β-OHB caused a slow decline in BS at a rate more rapid than with starvation alone. Insignificant increases in IRI (x9 μU) within 60 minutes were seen in 3 patients whereas the values of a control subject rose 65 μU within 20 minutes. Patient's values remained low throughout the test period in spite of progressively increasing ketosis. After the initial rise and fall, IRI slowly increased in the control subject at the 4th, 5th and 6th hours of infusion.
A 16-hour fast did not cause hypoglycemia in patients or control subjects. With heparin, NEFA and ketones increased to high levels. Three of 4 patients became hypoglycemic by the 16th hour (x BS 21 mg %). Failure of two patients to respond to i.v. glucagon suggests depleted liver glycogen. IRI levels were low throughout the test periods. Hypoglycemia may be due to failure of ketone stimulation of insulin production with concomitant preservation of liver glycogen. (APS).
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Sauls, H., Ulstrom, R. 77 Ketotic Hypoglycemia: The Effect of Beta-Hydroxy Butyrate (β-OHB) Infusion and Heparin-induced Ketosis. Pediatr Res 1, 220 (1967). https://doi.org/10.1203/00006450-196705000-00084
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DOI: https://doi.org/10.1203/00006450-196705000-00084