Birth weight concerning obesity and diabetes gene expression in healthy infants; a case-control study

Sahar Cheshmeh1, Shima Moradi2,3, Seyyed Mostafa Nachvak4

  • 1Molecular and Experimental Nutritional Medicine Department, University of Potsdam, Nuthetal, Germany.

Insights

Low birth weight infants show altered expression of key obesity and diabetes genes. Specifically, MTNR1B, NTRK2, PCSK1, and PTEN genes were upregulated, while the PPAR-a gene was downregulated in low birth weight (LBW) infants.

Area of Science:

  • Genetics and Molecular Biology
  • Pediatrics
  • Metabolic Disorders

Background:

  • Obesity and diabetes are global health concerns.
  • Identifying contributing factors is crucial for intervention.
  • Investigating gene expression in low birth weight (LBW) infants offers insight into metabolic disease risk.

Purpose of the Study:

  • To compare the expression of specific obesity and diabetes-related genes in infants with low birth weight (<2500g) versus normal birth weight.
  • To identify potential genetic markers associated with birth weight and metabolic health.

Main Methods:

  • A case-control study involving 215 healthy infants (5-6 months old).
  • Blood samples were collected to assess the expression of 16 key genes.
  • Statistical analyses included Chi-square, Mann-Whitney U, and Spearman correlation.

Main Results:

  • Significant inverse correlations were found between birth weight and the expression of MTNR1B, NTRK2, PCSK1, and PTEN genes.
  • These genes showed significantly higher expression levels in LBW infants compared to normal birth weight infants.
  • PPAR-a gene expression positively correlated with birth weight and was significantly upregulated in normal birth weight infants.

Conclusions:

  • LBW is associated with altered expression of genes involved in obesity and diabetes.
  • MTNR1B, NTRK2, PCSK1, and PTEN gene upregulation in LBW infants may indicate increased metabolic risk.
  • PPAR-a downregulation in LBW infants suggests potential metabolic dysregulation.
Abstract

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