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Am J Physiol Cell Physiol. 2017 Feb 1;312(2):C190-C197. doi: 10.1152/ajpcell.00298.2016. Epub 2016 Nov 30.

Changes in mitochondrial morphology and organization can enhance energy supply from mitochondrial oxidative phosphorylation in diabetic cardiomyopathy.

Author information

1
Cell Structure and Mechanobiology Group, Department of Mechanical Engineering, University of Melbourne, Parkville, Australia.
2
Systems Biology Laboratory, Melbourne School of Engineering, University of Melbourne, Parkville, Australia.
3
Department of Physiology, University of Melbourne, Parkville, Australia.
4
School of Biological Sciences, University of Auckland, Aukland, New Zealand.
5
School of Mathematics and Statistics, Faculty of Science, University of Melbourne, Parkville, Australia.
6
School of Medicine, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Parkville, Australia.
7
ARC Centre of Excellence in Convergent Bio-Nano Science and Technology, University of Melbourne, Parkville, Australia; and.
8
Advanced Microscopy Facility, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Parkville, Australia.
9
Cell Structure and Mechanobiology Group, Department of Mechanical Engineering, University of Melbourne, Parkville, Australia; vijay.rajagopal@unimelb.edu.au.

Abstract

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.

KEYWORDS:

cardiac ultrastructure; diabetic cardiomyopathy; mitochondrion dynamics; oxidative phosphorylation

PMID:
27903587
DOI:
10.1152/ajpcell.00298.2016
[Indexed for MEDLINE]
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