Pediatrics ·
Creatine metabolism is altered in necrotizing enterocolitis
A translational study combined intestinal cell and organoid experiments with analyses of human NEC tissue datasets and serial urine samples from preterm infants. Creatine supported epithelial repair and cellular energy production in experimental models, while creatine-related gene expression and urinary creatine were lower in association with NEC.
- Creatine improved epithelial repair and bioenergetic measures in experimental models.
- NEC tissue datasets showed lower expression of creatine metabolism genes.
- Urinary creatine declined at NEC diagnosis in preterm infants.
- Clinical benefit from supplementation has not been established.
Researchers examined creatine metabolism in necrotizing enterocolitis (NEC) using enterocyte wound-healing and metabolic assays, hypoxia-induced apoptosis experiments in human preterm ileal enteroids, human NEC transcriptomic datasets, and longitudinal urine samples from preterm infants collected before and at NEC diagnosis. The source does not report the number of infants or tissue samples analyzed.
In experimental models, creatine at 1–10 mM enhanced enterocyte wound healing, increased mitochondrial and glycolytic ATP production, and reduced hypoxia-associated apoptosis. Analyses of NEC tissue datasets showed lower expression of creatine metabolism genes across bulk samples and epithelial cell populations. Urinary creatine, but not related metabolites, declined significantly from baseline to NEC diagnosis.
The findings identify creatine depletion as a potential metabolic vulnerability in NEC and support further investigation of supplementation. However, the reported benefits come from cell and organoid experiments; the human findings are associative. The study does not establish that supplementation prevents or treats NEC in infants, and the source provides no sample sizes or clinical supplementation outcomes.
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Pediatric Research: Creatine metabolism is dysregulated in necrotizing enterocolitis ↗This is an automated AI-condensed summary that has not yet been reviewed by an editor. Always consult the full item at the original source.