Dietary or pharmacological inhibition of insulin-like growth factor-1 protects from renal ischemia-reperfusion injury in mice
2024

How Reducing Protein in Diets Helps Protect Kidneys from Injury

Sample size: 32 publication 10 minutes Evidence: high

Author Information

Author(s): Lyon Arnaud, Agius Thomas, Macarthur Michael R., Kiesworo Kevin, Stavart Louis, Allagnat Florent, Mitchell Sarah J., Riella Leonardo V., Uygun Korkut, Yeh Heidi, Déglise Sebastien, Golshayan Déla, Longchamp Alban

Primary Institution: Department of Vascular Surgery, Lausanne University Hospital (CHUV), University of Lausanne (UNIL), Lausanne, Switzerland

Hypothesis

Does short-term protein restriction reduce IGF-1 levels and protect against renal ischemia-reperfusion injury?

Conclusion

Reducing protein intake or blocking IGF-1 signaling can protect kidneys from damage during ischemia-reperfusion injury.

Supporting Evidence

  • Protein restriction significantly decreased IGF-1 levels in mice.
  • Exogenous IGF-1 administration increased renal injury during ischemia-reperfusion.
  • Pharmacological inhibition of IGF-1 signaling improved survival rates after kidney injury.
  • Short-term dietary changes can have significant effects on kidney health.

Takeaway

Eating less protein can help your kidneys stay healthy, especially when they are hurt. It's like giving them a break to heal better.

Methodology

Mice were fed diets with varying protein levels and subjected to renal ischemia-reperfusion injury to assess the effects of protein restriction and IGF-1 signaling inhibition.

Potential Biases

Potential bias due to the use of a single animal model and the specific dietary interventions applied.

Limitations

The study's findings may be limited by the dual inhibition of IGF-1R and insulin receptor by linsitinib, making it hard to separate their effects.

Participant Demographics

10-week-old male and female C57BL/6J mice, and 18-month-old male mice.

Statistical Information

P-Value

0.0017

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1016/j.isci.2024.111256

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