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Updated: Jul 13, 2026

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
Published on: November 29, 2024
Mouse model of erectile dysfunction due to diet-induced diabetes mellitus
Donghua Xie1, Shelley I Odronic, Feihua Wu
1Division of Cardiology, Department of Medicine, Durham Veterans Affairs and Duke University Medical Center, Durham, North Carolina 27710, USA.
Objectives:
To determine whether diet-induced diabetes mellitus (DM) in mice would reproduce the major features of human erectile dysfunction (ED) because DM is a significant risk factor in the development of ED.
Methods:
In total, 150 C57BL6 (bl6) mice were divided into six groups of 25 mice each. Of these 150 mice, 125 were fed a high-fat (45% of total calories) diet for the final 4 (group 2), 8 (group 3), 12 (group 4), 16 (group 5), or 22 (group 6) weeks. Group 1 was fed a normal diet. The mice were 22 to 25 weeks old at study termination. The corporal tissues were harvested and studied for endothelium-dependent and endothelium-independent vasoreactivity, endothelial and smooth muscle cell content by immunohistochemistry, nitric oxide synthase expression by nicotinamide adenine dinucleotide-diaphorase staining, and apoptosis by terminal deoxynucleotidyl transferase biotin-D-UTP nick-end labeling staining.
Results:
The blood glucose levels were greater in groups 2 to 6 compared with those in group 1. The vasoreactivity, endothelial cell content, and smooth muscle/collagen ratio were lower and apoptosis were greater in the DM mice (P = 0.0001, P = 0.10, P = 0.0002, P <0.001, and P <0.001, respectively). Significantly decreased nitric oxide synthase expression and significantly increased apoptosis (P <0.0001 each) was found in the high-fat diet mice.
Conclusions:
Corporal tissue from mice with diet-induced DM demonstrated many of the major functional, structural, and biochemical changes found in humans with ED. This model should serve as a valuable tool for advancing our understanding of the role DM plays in the pathogenesis of ED.
Insights
Diet-induced diabetes mellitus in mice mimics human erectile dysfunction, showing similar functional and structural changes. This mouse model is crucial for understanding diabetes
Area of Science:
- Urology
- Endocrinology
- Diabetology
Background:
- Diabetes mellitus (DM) is a significant risk factor for erectile dysfunction (ED).
- Understanding the mechanisms linking DM and ED is crucial for developing effective treatments.
Purpose of the Study:
- To establish a mouse model of diet-induced DM that replicates key features of human ED.
- To investigate the functional, structural, and biochemical changes in corporal tissue associated with DM-induced ED.
Main Methods:
- 150 C57BL6 mice were divided into six groups; 125 received a high-fat diet for varying durations (4-22 weeks), while one control group received a normal diet.
- Corporal tissues were analyzed for vasoreactivity, cell content (endothelial, smooth muscle), nitric oxide synthase (NOS) expression, and apoptosis.
Main Results:
- Mice on high-fat diets exhibited elevated blood glucose levels, confirming diet-induced diabetes mellitus.
- DM mice showed impaired vasoreactivity, reduced endothelial cell content, altered smooth muscle/collagen ratio, and increased apoptosis.
- Significantly decreased NOS expression and increased apoptosis were observed in high-fat diet-induced DM mice.
Conclusions:
- Diet-induced DM in mice successfully reproduced major functional, structural, and biochemical alterations seen in human ED.
- This mouse model provides a valuable platform for further research into the pathogenesis of DM-related ED.
