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LEAP2 deficiency does not impair essential iron-dependent functions in zebrafish
Yueyue Fei1, Chongyu Zhong1, Ruiqin Hu2
1Key Laboratory of Marine Genetic Resources and Breeding, Jiangsu Ocean University, Lianyungang, Jiangsu, China.
Fish & Shellfish Immunology
|October 12, 2025
Summary
Liver-expressed antimicrobial peptide 2 (LEAP2) deficiency in zebrafish did not disrupt iron metabolism but may worsen ferroptosis during infection by altering ferritin levels. This study clarifies LEAP2's biological function.
Area of Science:
- Biochemistry
- Molecular Biology
- Zebrafish Models
Background:
- Liver-expressed antimicrobial peptide 2 (LEAP2) is a blood-derived peptide with a controversial metabolic role.
- LEAP2 shares characteristics with LEAP1/hepcidin, a key regulator of iron metabolism.
- Understanding LEAP2's function is crucial for metabolic research.
Purpose of the Study:
- To investigate the effects of LEAP2 deficiency on metabolism in zebrafish.
- To analyze iron metabolism, hemoglobin levels, erythrocyte counts, and ferritin expression in LEAP2 knockout zebrafish.
- To determine LEAP2's role in response to bacterial infection.
Main Methods:
- Utilized a LEAP2 knockout zebrafish model.
- Performed comprehensive analyses of tissue iron content, hemoglobin, erythrocyte counts, and ferritin expression.
- Assessed metabolic changes and response to Aeromonas hydrophila infection.
Main Results:
- LEAP2 knockout zebrafish embryos showed developmental retardation.
- No significant alterations in systemic iron homeostasis (hemoglobin, erythrocytes, tissue iron) were observed.
- Liver ferritin increased, intestinal ferritin decreased, and liver ferritin reduced upon infection.
Conclusions:
- LEAP2 deficiency does not significantly disrupt systemic iron homeostasis in zebrafish.
- LEAP2 deficiency may exacerbate ferroptosis under bacterial infection by modulating ferritin metabolism.
- This study provides novel insights into the biological function of LEAP2.
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