Key result
Type 1 diabetes in OVE26 mice reduced the mitochondrial respiratory control ratio (6.13 vs 9.63, P<0.0001) and GSH levels, indicating impaired mitochondrial function and increased oxidative stress.
Population
OVE26 mouse model of type 1 diabetes
Comparison
Type 1 diabetes (disease model) vs Non-diabetic controls
Design
Preclinical
Authors
Loading...
Mitochondrial protein shifts in diabetic mouse hearts remain hypothesis-generating; leaves open relevance to human cardiomyopathy therapies.
Absolute Event Rate: 6.13% vs 9.63%
p-value: p=< 0.0001
In a mouse model of type 1 diabetes, cardiac mitochondria exhibit significant damage, impaired function, and increased oxidative stress, which coincides with stimulated mitochondrial biogenesis.
Shen et al. (2004) studied Type 1 diabetes and diabetic cardiomyopathy. Type 1 diabetes vs. Non-diabetic controls was evaluated on Respiratory control ratio (p=< 0.0001). Type 1 diabetes in OVE26 mice reduced the mitochondrial respiratory control ratio (6.13 vs 9.63, P<0.0001) and GSH levels, indicating impaired mitochondrial function and increased oxidative stress.
Synapse has enriched 3 closely related papers on similar clinical questions. Consider them for comparative context: