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Iron Stress Reprograms Enterocyte Metabolism.

Shya E Navazesh1, Peng Ji1

  • 1Department of Nutrition, University of California Davis, 1 Shields Ave., Davis, CA 95616, USA.

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Summary
This summary is machine-generated.

Iron deficiency impairs enterocyte proliferation and disrupts cellular metabolism, while excess iron affects cholesterol synthesis and vitamin E levels. Iron repletion partially restores metabolic function, showing enterocyte resilience.

Keywords:
IPEC-J2 cellsenterocyteintestinal inflammationiron deficiencyiron excessuntargeted metabolomics

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Area of Science:

  • Cell Biology
  • Nutritional Science
  • Gastroenterology

Background:

  • Enterocyte metabolism and inflammatory responses are crucial for gut health.
  • Iron homeostasis is vital for cellular function, and its dysregulation can lead to various pathologies.
  • Understanding the impact of iron deficiency and excess on enterocytes is essential for managing gastrointestinal disorders.

Purpose of the Study:

  • To investigate the effects of iron deficiency (ID) and iron excess (IE) on enterocyte metabolism and inflammatory marker transcription.
  • To analyze the interplay between iron imbalance, lipopolysaccharide (LPS) exposure, and inflammatory gene expression.
  • To characterize the metabolic shifts in enterocytes under conditions of ID, IE, and iron repletion.

Main Methods:

  • Utilized IPEC-J2 cells, a neonatal pig jejunum-derived cell line.
  • Induced ID and IE using deferiprone (DFP) and ferric ammonium citrate (FAC), respectively.
  • Employed transcriptional analysis, LPS challenge, and untargeted metabolomics to assess cellular responses.

Main Results:

  • ID suppressed proliferation and disrupted the TCA cycle, glucuronic acid synthesis, and glycolysis.
  • IE reduced transferrin receptor (TFRC) expression, increased cholesterol biosynthesis, and depleted alpha-tocopherol.
  • LPS and ID synergistically upregulated inflammatory markers like IL8.
  • Iron repletion partially reversed ID-induced metabolic alterations.

Conclusions:

  • Iron deficiency profoundly disrupts enterocyte metabolism and proliferation.
  • Iron excess alters lipid metabolism and antioxidant levels in enterocytes.
  • Enterocytes exhibit resilience, with partial restoration of metabolic function upon iron repletion.