Kidney Week

Abstract: FR-PO160

Time-Restricted Feeding Protects against Kidney Ischemia-Reperfusion Injury in Mice

Session Information

• AKI: Mechanisms
  October 25, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 103 AKI: Mechanisms

Authors

• Jang, Yoonjoo, Pusan National University Yangsan Hospital, Yangsan, Korea (the Republic of)

Yoonjoo Jang, MD

• Ye, Byung Min, Pusan National University Yangsan Hospital, Yangsan, Korea (the Republic of)

Byung Min Ye, MD

• Kim, Seo Rin, Pusan National University Yangsan Hospital, Yangsan, Korea (the Republic of)

Seo Rin Kim, MD

• Kim, Il Young, Pusan National University Yangsan Hospital, Yangsan, Korea (the Republic of)

Il Young Kim, MD

• Lee, Dong Won, Pusan National University Yangsan Hospital, Yangsan, Korea (the Republic of)

Dong Won Lee, MD, PhD

• Lee, Soo Bong, Pusan National University Yangsan Hospital, Yangsan, Korea (the Republic of)

Soo Bong Lee, MD, PhD

Background

Ischemia–reperfusion injury (IRI) in the kidneys stands as a significant contributor to acute kidney injury (AKI). Time-restricted feeding (TRF), known for its metabolic health benefits and alleviation of various chronic diseases without calorie restriction, was investigated for its potential protective effects against IRI-induced AKI.

Methods

C57BL/6 male mice underwent unilateral IRI, and their kidneys were harvested after 2 days. Mice assigned to the TRF group had unrestricted access to standard chow daily but were restricted to an 8-hour feeding window during the dark cycle for two weeks prior to IRI induction. The mice were categorized into four groups: Control, TRF, IRI, and TRF + IRI.

Results

In the TRF + IRI mice, there was a significant reduction observed in the tubular damage score compared to the IRI group. Additionally, the TRF + IRI mice displayed decreased levels of phosphorylated NF-κB and F4/80-positive macrophages relative to the IRI mice. Moreover, markers denoting oxidative stress for protein, lipid and DNA were notably diminished in the TRF + IRI mice in comparison to the IRI mice. Furthermore, TUNEL-positive tubular cells and cleaved caspase-3 expression were observed at lower levels in the TRF + IRI group than in the IRI group.

Conclusion

TRF, without the imposition of calorie restriction, effectively mitigated renal damage by attenuating inflammatory reactions, oxidative stress, and tubular apoptosis in an experimental model of renal IRI. This underscores TRF's potential as an innovative dietary strategy for averting IRI-induced AKI.