Key result
Streptozotocin-induced diabetes reduced mitochondrial state 3 respiration to 59.1% of control, and complex I and V activities to 43.4% and 71.7%, all of which recovered with insulin treatment.
Why the study?
Does insulin treatment improve mitochondrial respiratory impairment in streptozotocin-induced diabetic rat hearts?
Does insulin treatment improve mitochondrial respiratory impairment in streptozotocin-induced diabetic rat hearts?
In a diabetic rat model, impaired oxidative phosphorylation due to depressed complex I and V activities contributes to cardiac mitochondrial dysfunction, which is reversible with insulin treatment.
Answers are grounded in this paper and cite their sources.
Insulin may restore mitochondrial function in diabetic rat hearts; hypothesis-generating and should not change practice.
The purpose of this study was to examine mitochondrial respiratory impairment in the diabetic heart. Diabetes mellitus was induced in male Wistar rats by intravenous injection of streptozotocin (STZ) for 2 to 16 weeks (Group D). In some of the diabetic rats, insulin was injected for 2 or 3 weeks prior to sacrifice (Group I). Fasting blood glucose was markedly elevated to greater than 300 mg/dl in Group D and was similar to normal glucose levels in Group I. At 2 weeks after STZ injection, state 3 was only 59.1% of that in the control. Complex I and complex V activities were also significantly reduced to 43.4% and 71.7% of those in the control, respectively. These reductions recovered with insulin treatment. This phenomenon persisted for 16 weeks. Morphological studies revealed swelling of the mitochondria and an increase in lipid droplets in diabetic cardiomyocytes, and these were also improved with insulin treatment. We conclude that in the diabetic heart, disturbance of energy production in cardiac mitochondria is generated by the impairment of oxidative phosphorylation due to depression of complex I and complex V. These changes may contribute the cardiac dysfunction that is a complication of diabetes mellitus.
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Tomita et al. (1996) studied Diabetes mellitus. Streptozotocin (STZ) vs. Control and insulin-treated diabetic rats was evaluated on Mitochondrial state 3 respiration. Streptozotocin-induced diabetes reduced mitochondrial state 3 respiration to 59.1% of control, and complex I and V activities to 43.4% and 71.7%, all of which recovered with insulin treatment.
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