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Updated: May 25, 2026

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
10:31

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

Published on: May 2, 2025

Catalase deficiency accelerates diabetic renal injury through peroxisomal dysfunction

Inah Hwang1, Jiyoun Lee, Joo Young Huh

  • 1Department of Bioinspired Science, Division of Life and Pharmaceutical Sciences, Center for Cell Signaling and Drug Discovery Research, College of Pharmacy, Ewha Womans University, Seoul, Korea.

Diabetes
|February 9, 2012
PubMed

Insights

Catalase deficiency worsens diabetic kidney disease (DKD) by impairing peroxisomal function and free fatty acid (FFA) metabolism. This leads to increased oxidative stress and kidney damage, highlighting catalase

Area of Science:

  • Nephrology
  • Metabolic Disorders
  • Oxidative Stress Research

Background:

  • Mitochondrial reactive oxygen species (ROS) contribute to diabetic complications like diabetic nephropathy (DN).
  • Increased plasma free fatty acids (FFAs) and glucose in diabetes involve peroxisomes and mitochondria in FFA oxidation.
  • Catalase, a key peroxisomal antioxidant, is investigated for its role in protecting kidneys during diabetes.

Purpose of the Study:

  • To investigate if catalase deficiency accelerates diabetic nephropathy (DN) via peroxisomal dysfunction and altered renal FFA metabolism.
  • To elucidate the protective role of endogenous catalase in the kidney against diabetic stress.

Main Methods:

  • Diabetes was induced in catalase knock-out (CKO) and wild-type (WT) mice using streptozotocin.
  • Murine mesangial cells (MMCs) were used to study the effects of catalase deficiency and re-expression.
  • Parameters of DN, oxidative stress markers, peroxisomal/mitochondrial function, and FFA oxidation were assessed.

Main Results:

  • Diabetic CKO mice exhibited accelerated DN and oxidative stress compared to diabetic WT mice, despite similar hyperglycemia.
  • Catalase deficiency impaired peroxisomal/mitochondrial biogenesis and FFA oxidation in both CKO mice and MMCs.
  • FFAs induced mitochondrial ROS and fibronectin expression in CKO mice and MMCs, which were ameliorated by catalase re-expression or N-acetylcysteine.

Conclusions:

  • FFA-induced peroxisomal dysfunction exacerbates diabetic nephropathy (DN).
  • Endogenous catalase is crucial for protecting the kidney from diabetic stress.
  • Maintaining peroxisomal and mitochondrial fitness is essential for kidney protection in diabetes.

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