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Leucine kinetics during simultaneously administered insulin and dexamethasone in preterm infants with severe lung

R H van Beek1, L J Zimmermann, J G Vergunst van Keulen

  • 1Department of Pediatrics, Ignatius Hospital Breda, 4800 RK Breda, The Netherlands.

Pediatric Research
|March 3, 2001
PubMed

Insights

Insulin did not prevent the catabolic effects of dexamethasone in preterm infants with chronic lung disease. Leucine metabolism remained unchanged, but weight gain decreased during treatment.

Area of Science:

  • Biochemistry
  • Neonatology
  • Pediatric Endocrinology

Background:

  • Dexamethasone is known to cause catabolic effects in preterm infants with chronic lung disease.
  • Insulin is an anabolic hormone that may counteract these effects.

Purpose of the Study:

  • To investigate if insulin administration can prevent the catabolic effects of dexamethasone in very-low-birth-weight infants with chronic lung disease.
  • To assess the impact of insulin on leucine metabolism during dexamethasone treatment.

Main Methods:

  • A study involving 11 very-low-birth-weight infants receiving dexamethasone treatment.
  • Leucine metabolism was measured before and on days 2, 4, and 7 of dexamethasone administration.
  • Insulin was administered intravenously at doses of 0.5 or 1.0 IU/kg/d during the first 4 days of dexamethasone treatment.

Main Results:

  • Leucine turnover and breakdown showed no significant changes during insulin and dexamethasone administration.
  • Weight gain rates were significantly lower during the first week of dexamethasone treatment compared to other periods.
  • The observed decrease in weight gain was not reversed by insulin administration.

Conclusions:

  • Insulin administration did not alter leucine kinetics in very-low-birth-weight infants receiving dexamethasone.
  • The catabolic effects of dexamethasone, indicated by reduced weight gain, were not mitigated by concurrent insulin therapy.
  • Further research may be needed to explore alternative strategies for managing dexamethasone-induced catabolism in this population.

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