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Paper of the Month-(May 2018) from Drs. Chris Perry and Thomas Hawke research group

Paper of the Month-(May 2018) from Drs. Chris Perry and Thomas Hawke research group

Monaco CMF, Hughes MC, Ramos SV, Varah NE, Lamberz C, Rahman FA, McGlory C, Tarnopolsky MA, Krause MP, Laham R, Hawke TJ, Perry CGR. Altered mitochondrial bioenergetics and ultrastructure in the skeletal muscle of young adults with type 1 diabetes. Diabetologia. 2018 Apr 18. doi: 10.1007/s00125-018-4602-6

From the authors:

Skeletal muscle, by virtue of its mass and its high capacity to burn sugar as a fuel, is perhaps the main determinate of blood sugar control in diabetes. Impairments to the mitochondria (the powerhouse of the cell) found within skeletal muscle have been implicated in the progression of a number of diseases including type 2 diabetes and cancer cachexia. However, whether the mitochondria in skeletal muscle are adversely affected in physically-active young adults with type 1 diabetes has yet to be determined.  If present (and left unchecked), these changes could affect the ability to manage blood glucose levels and may be responsible for the more rapid onset of disability with advancing age.

In a recent publication in Diabetologia (link below), a leading diabetes research journal, we show that type 1 diabetes can be associated with a reduction in the ability of mitochondria to generate energy, while at the same time, increasing the amount of oxidative stress within the muscle.  The changes lead to visible increases in ‘debris’ within the skeletal muscle of those with type 1 diabetes.  Despite these negative alterations, we did not see evidence of a loss of mitochondrial or blood vessel content in the muscle, suggesting that it is the quality of the mitochondria that is likely impacted by the disease condition. Given that our subjects were self-reporting physical activity levels that exceed the recent Diabetes Canada Clinical Practise Guideline on physical activity (link below), it is likely that their level of activity was preventing the full extent of impairments that would exist were they leading an inactive (sedentary) lifestyle.

Taken together, our findings indicate that the current exercise guidelines for those with type 1 diabetes may be insufficient to fully prevent skeletal muscle metabolic abnormalities in young adults and further research is needed to identify therapeutic strategies (e.g. optimal exercise prescription) that can maximize muscle health in those with type 1 diabetes.

Click here to view a PDF document of this article.