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Related Experiment Video

Updated: Dec 22, 2025

Author Spotlight: Enhancing Understanding and Treatment Strategies with the NEC-on-a-Chip Model

Author Spotlight: Enhancing Understanding and Treatment Strategies with the NEC-on-a-Chip Model

Published on: July 28, 2023

Progressive Metabolic Dysfunction and Nutritional Variability Precedes Necrotizing Enterocolitis.

Tiffany J Sinclair^1,2, Chengyin Ye³, Yunliang Chen^1,4

¹Department of Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.

|May 6, 2020

Summary

This summary is machine-generated.

Necrotizing enterocolitis (NEC) in premature infants is linked to early metabolic differences and nutritional deficits. Metabolic dysfunction progresses with altered nutrient delivery, offering insights into NEC prevention.

Keywords:

growth faltering growth velocity metabolomics necrotizing enterocolitis newborn calories newborn metabolic profiling prematurity very low birthweight

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Area of Science:

Neonatal Medicine
Metabolomics
Nutritional Science

Background:

Necrotizing enterocolitis (NEC) is a severe gastrointestinal condition primarily affecting preterm infants.
It is associated with prematurity, enteral feeding practices, and alterations in gut microbiota (dysbiosis).
Existing knowledge suggests nutritional variability and metabolic dysfunction may precede NEC onset.

Purpose of the Study:

To investigate the association between metabolic profiles (amino acids and acylcarnitines) and nutritional intake with the development of NEC in preterm infants.
To identify specific metabolites and nutritional patterns that predict NEC onset.
To explore the longitudinal progression of metabolic changes in relation to NEC.

Main Methods:

A multicenter longitudinal study involving 995 preterm infants (<32 weeks gestation), with 73 diagnosed with NEC.
Dried blood spot samples analyzed for 72 amino acids (AA) and acylcarnitines (AC) on days 1, 7, 28, and 42.
Nutritional data, including weight-adjusted total calories, were collected concurrently.
Statistical analysis included odds ratios and longitudinal plotting to assess associations with NEC.

Main Results:

Specific Day 1 metabolites (e.g., alanine, phenylalanine, free carnitine) were associated with subsequent NEC development.
Metabolite profiles shifted from predominantly AAs at birth to ACs by day 42 in infants who developed NEC.
Infants with NEC received significantly lower weight-adjusted total calories starting from day 7 through day 42.

Conclusions:

Preterm infants exhibit distinct metabolic profiles at birth that are associated with NEC.
Metabolic abnormalities progress in parallel with suboptimal nutritional delivery, indicating metabolic dysfunction prior to NEC.
These findings offer novel insights into NEC pathophysiology and potential avenues for clinical prevention strategies.