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Inborn Errors of Metabolism01:20

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Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
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Published on: November 20, 2015

Prematurity and programming: are there later metabolic sequelae?

Paul L Hofman1, Fiona Regan, Craig A Jefferies

  • 1Liggins Institute, University of Auckland, Auckland, New Zealand.

Metabolic Syndrome and Related Disorders
|March 29, 2008
PubMed
Summary
This summary is machine-generated.

Premature birth is linked to insulin resistance and metabolic syndrome risk, similar to term small-for-gestational-age infants. Epigenetic changes may explain this increased risk in preterm children.

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Area of Science:

  • Pediatrics
  • Endocrinology
  • Metabolic Health

Background:

  • Low birth weight is associated with early insulin resistance and later metabolic syndrome.
  • Most research focuses on term low-birth-weight infants, neglecting other groups.
  • Prematurely born children represent a significant low-birth-weight population requiring evaluation.

Purpose of the Study:

  • To review the metabolic profile of prematurely born children.
  • To assess the risk of metabolic syndrome in this population.
  • To explore potential mechanisms, including epigenetic alterations, linking preterm birth to metabolic dysfunction.

Main Methods:

  • Literature review focusing on metabolic profiles of preterm infants.
  • Comparison of metabolic characteristics between preterm and term small-for-gestational-age (SGA) children.
  • Exploration of proposed mechanisms such as epigenetic alterations and hypomethylation.

Main Results:

  • Prematurely born children exhibit a metabolic profile similar to term SGA children.
  • This similarity suggests a potentially comparable increased risk for metabolic syndrome later in life.
  • Epigenetic alterations, particularly hypomethylation, are proposed as key mechanisms.

Conclusions:

  • Premature birth may confer a similar metabolic syndrome risk as term SGA.
  • Epigenetic modifications are a plausible pathway for this increased risk.
  • Further research into preterm infants' long-term metabolic health is warranted.