Physical activity is the key determinant of skeletal muscle mitochondrial function in type 2 diabetes

Journal article


van Tienen, F. H. J., Praet, Stephan F. E., de Feyter, H. M., van Den Broek, N. M., Lindsey, P. J., Schoonderwoerd, K. G. C., de Coo, I. F. M., Nicolay, K., Prompers, J. J., Smeets, H. J. M. and van Loon, Luc J. C.. (2012). Physical activity is the key determinant of skeletal muscle mitochondrial function in type 2 diabetes. The Journal of Clinical Endocrinology and Metabolism. 97(9), pp. 3261 - 3269. https://doi.org/10.1210/jc.2011-3454
Authorsvan Tienen, F. H. J., Praet, Stephan F. E., de Feyter, H. M., van Den Broek, N. M., Lindsey, P. J., Schoonderwoerd, K. G. C., de Coo, I. F. M., Nicolay, K., Prompers, J. J., Smeets, H. J. M. and van Loon, Luc J. C.
Abstract

Context: Conflicting data exist on mitochondrial function and physical activity in type 2 diabetes mellitus (T2DM) development. Objective: The aim was to assess mitochondrial function at different stages during T2DM development in combination with physical exercise in longstanding T2DM patients. Design and Methods: We performed cross-sectional analysis of skeletal muscle from 12 prediabetic 11 longstanding T2DM male subjects and 12 male controls matched by age and body mass index. Intervention: One-year intrasubject controlled supervised exercise training intervention was done in longstanding T2DM patients. Main Outcome Measurements: Extensive ex vivo analyses of mitochondrial quality, quantity, and function were collected and combined with global gene expression analysis and in vivo ATP production capacity after 1 yr of training. Results: Mitochondrial density, complex I activity, and the expression of Krebs cycle and oxidative phosphorylation system-related genes were lower in longstanding T2DM subjects but not in prediabetic subjects compared with controls. This indicated a reduced capacity to generate ATP in longstanding T2DM patients only. Gene expression analysis in prediabetic subjects suggested a switch from carbohydrate toward lipid as an energy source. One year of exercise training raised in vivo skeletal muscle ATP production capacity by 21 ± 2% with an increased trend in mitochondrial density and complex I activity. In addition, expression levels of β-oxidation, Krebs cycle, and oxidative phosphorylation system-related genes were higher after exercise training. Conclusions: Mitochondrial dysfunction is apparent only in inactive longstanding T2DM patients, which suggests that mitochondrial function and insulin resistance do not depend on each other. Prolonged exercise training can, at least partly, reverse the mitochondrial impairments associated with the longstanding diabetic state.

Year2012
JournalThe Journal of Clinical Endocrinology and Metabolism
Journal citation97 (9), pp. 3261 - 3269
PublisherOxford University Press
ISSN0021-972X
Digital Object Identifier (DOI)https://doi.org/10.1210/jc.2011-3454
Scopus EID2-s2.0-84866181138
Page range3261 - 3269
Research GroupMary MacKillop Institute for Health Research
Publisher's version
File Access Level
Controlled
Place of publicationUnited States
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