Key result
In diabetic cardiomyocytes, mitochondria were 20% smaller with a 53% increase in spatial density and formed larger clusters, which may enhance cytosolic ATP availability.
Structural changes in mitochondria during diabetic cardiomyopathy, including increased clustering and surface-to-volume ratio, may serve as a compensatory mechanism to enhance cytosolic ATP availability.
Highlights potential mitochondrial adaptations in diabetic cardiomyopathy; hypothesis-generating and should not yet inform clinical practice.
Diabetic cardiomyopathy is accompanied by metabolic and ultrastructural alterations, but the impact of the structural changes on metabolism itself is yet to be determined. Morphometric analysis of mitochondrial shape and spatial organization within transverse sections of cardiomyocytes from control and streptozotocin-induced type I diabetic Sprague-Dawley rats revealed that mitochondria are 20% smaller in size while their spatial density increases by 53% in diabetic cells relative to control myocytes. Diabetic cells formed larger clusters of mitochondria (60% more mitochondria per cluster) and the effective surface-to-volume ratio of these clusters increased by 22.5%. Using a biophysical computational model we found that this increase can have a moderate compensatory effect by increasing the availability of ATP in the cytosol when ATP synthesis within the mitochondrial matrix is compromised.
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Jarosz et al. (2016) studied Diabetic cardiomyopathy. Streptozotocin-induced type I diabetes vs. Control was evaluated on Mitochondrial morphology and spatial organization. In diabetic cardiomyocytes, mitochondria were 20% smaller with a 53% increase in spatial density and formed larger clusters, which may enhance cytosolic ATP availability.
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