Rapid glucose disappearance in infants with infection
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Neonatal infection causes rapid glucose metabolism, with glucose disappearing faster even after recovery. This altered carbohydrate metabolism persists for weeks, and the cause remains unknown.
Area of Science:
- Neonatal Medicine
- Endocrinology
- Metabolic Research
Background:
- Neonatal infections are known to alter carbohydrate metabolism.
- Previous studies suggest rapid glucose disappearance during infection episodes.
Purpose of the Study:
- To quantify glucose disappearance rates during neonatal infection.
- To investigate the role of insulin and growth hormone in this altered metabolism.
- To determine the duration of metabolic abnormalities post-infection.
Main Methods:
- Intravenous glucose tolerance tests (IVGTT) were performed on infected neonates during acute illness and convalescence.
- Serial plasma insulin and growth hormone levels were measured.
- Data were compared to healthy control infants.
Main Results:
- Glucose disappearance rates (K1) were significantly increased in infected neonates compared to controls (p < 0.01).
- This rapid glucose disposal persisted for 5-15 days into convalescence.
- No significant differences in baseline or stimulated insulin and growth hormone levels were observed between groups.
Conclusions:
- Neonatal infection leads to rapid glucose utilization, independent of insulin or growth hormone levels.
- The disturbance in carbohydrate homeostasis is prolonged, lasting weeks after infection onset.
- The underlying cause of altered carbohydrate metabolism in neonatal infections remains unidentified.
Abstract:
Altered carbohydrate metabolism has been reported during episodes of neonatal infection. To document that there is more rapid glucose disappearance during infection, intravenous glucose tolerance tests (IVGTT) and serial plasma growth hormone and insulin levels were determined in eight full-term neonates during the first three days of an acute episode of infection and during convalescence, 5 to 15 days later. Eight healthy infants were each studied once using the same study protocol. Glucose disappearance rates, measured as K1 of glucose, were increased (p less than 0.01) during both the acute septic period (3.7 +/- 0.3% disappearance/min; mean +/- S.E.M.) and convalescent period (2.5 +/- 0.2% min) when compared with values in control infants (1.3 +/- 0.3%/min). Gram-negative, gram-positive, and viral infections were all associated with rapid glucose disposal. The abnormality in carbohydrate homeostasis persisted for at least 5 to 15 days after treatment was begun. Baseline and stimulated (20-minutes post bolus glucose infusion) plasma insulin and growth hormone levels did not differ among the groups. Thus, there is no evidence that hyperinsulinism produced the rapid glucose disappeared rate and enhanced glucose utilization. The reason for the disturbed carbohydrate metabolism in neonatal infections remains unknown.