Key result
TSOD mice exhibited no deterioration of cardiac function despite long-term severe obesity and diabetes, showing significantly higher ejection fraction than non-diabetic controls.
Why the study?
Does the Tsumura Suzuki Obese Diabetes (TSOD) mouse model exhibit impaired cardiovascular and endothelial function compared to non-diabetic controls?
Does the Tsumura Suzuki Obese Diabetes (TSOD) mouse model exhibit impaired cardiovascular and endothelial function compared to non-diabetic controls?
The TSOD mouse model of Type 2 diabetes does not develop cardiovascular or endothelial dysfunction up to 18 months of age, despite severe obesity and metabolic derangements.
Answers are grounded in this paper and cite their sources.
TSOD mice preserve cardiac function despite obesity/diabetes; challenges diabetic cardiomyopathy model assumptions and leaves open human translational relevance.
Diabetes mellitus is a well known and important risk factor for cardiovascular diseases, including heart failure. A new model of Type 2 diabetes, Tsumura Suzuki Obese Diabetes (TSOD) mice, was introduced recently into the research field of diabetes. The cardiac functions of TSOD mice were studied in comparison with Tsumura Suzuki Non Obesity (TSNO, non-diabetic control) mice, for the first time. In vivo cardiovascular functions were measured by echocardiography and cardiac catheterization at 7, 12 and 18 months old. TSOD mice had no deterioration of cardiac function despite the long-term persistence of severe obesity, hyperglycemia, hyperinsulinemia and hyperlipidemia, including high density lipoprotein (HDL)-cholesterol. No histopathological abnormalities were observed in the heart of TSOD mice, while several histological abnormalities were observed in the pancreas and kidney of TSOD mice. To investigate vascular endothelium function at 7 months old, intravenous injection of acetylcholine (ACh; 1, 3, 10 microg/kg)- and N(G)-nitro-L-arginine methyl ester (L-NAME; 50 mg/kg)-induced mean blood pressure (BP) changes were used. ACh decreased whereas L-NAME increased BP, and no significant differences in BP changes were observed between TSOD and TSNO mice. Moreover, ACh-induced relaxation of the thoracic aortae isolated from TSOD and TSNO mice with intact endothelium were not significantly different. These findings suggest that vascular endothelial cells in TSOD mice are not impaired. It was clearly demonstrated that despite obvious diabetes, cardiac functions of TSOD mice were not impaired even at 18 months old.
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Kawada et al. (2010) studied Type 2 diabetes (animal model). Tsumura Suzuki Obese Diabetes (TSOD) phenotype vs. Tsumura Suzuki Non Obesity (TSNO) mice was evaluated on Left ventricular ejection fraction at 12 months (p=<0.01). TSOD mice exhibited no deterioration of cardiac function despite long-term severe obesity and diabetes, showing significantly higher ejection fraction than non-diabetic controls.
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