Related Experiment Video
Updated: May 25, 2026
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
Summary
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.
Related Concept Videos
01:28Diabetic Nephropathy
Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...
01:27Diabetic Retinopathy
DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...
01:22Diabetic Ketoacidosis ll: Pathophysiology
Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...
01:24Peroxisomes
Peroxisomes are specialized organelles present in fungi, plant, and animal cells. It can vary in number, size, morphology, and activity depending on the type of tissue and the nutritional state of the cell. For example, cells with active lipid metabolism, such as adipocytes, neurons, and hepatocytes, have more peroxisomes than other cells in the body. Besides their primary role in breaking down complex organic molecules, peroxisomes can also synthesize specific macromolecules and participate in...
01:30Peroxisomes and Mitochondria
Peroxisomes and mitochondria are two important oxygen-utilizing organelles in eukaryotic cells. Mitochondria carry out cellular respiration—the process that converts energy from food into ATP. Peroxisomes carry out a variety of functions, primarily breaking down different substances, such as fatty acids.
The peroxisome is a single membrane-bound cellular organelle that can perform several different functions, including lipid metabolism and chemical detoxification. The enzymes within peroxisomes...
The peroxisome is a single membrane-bound cellular organelle that can perform several different functions, including lipid metabolism and chemical detoxification. The enzymes within peroxisomes...
01:27Protein Import into the Peroxisomes
Cells contain membrane-bound organelles called peroxisomes that oxidize organic molecules by transferring hydrogen atoms to oxygen, producing hydrogen peroxide. Peroxisomes enzymatically convert the released hydrogen peroxide into water and oxygen.
Peroxisomal Protein Import:
Peroxisomes lack the genetic machinery required to code for their own proteins. Hence, most peroxisomal membrane, lumenal and transmembrane proteins are synthesized in the cytoplasm or ER and transported to the peroxisome...
Peroxisomal Protein Import:
Peroxisomes lack the genetic machinery required to code for their own proteins. Hence, most peroxisomal membrane, lumenal and transmembrane proteins are synthesized in the cytoplasm or ER and transported to the peroxisome...