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Physical exercise in the treatment of type 2 diabetes
2 March 2010
Participation in a 12-week physical exercise program restores mitochondrial function in patients with type 2 diabetes. The increase in mitochondrial function is paralleled by increased glucose uptake and restoration of the ability to adapt glucose- and fat oxidation to fuel availability. This is shown by recent research performed by M.Sc. Ruth Meex within the research team of dr. Matthijs Hesselink, dr. Patrick Schrauwen and colleagues from the School of Nutrition and Metabolism Maastricht (NUTRIM), Maastricht University. These data are published in the March issue of Diabetes, the leading journal in the field.
Patients with type 2 diabetes are characterised by reduced glucose uptake in the muscle and compromised mitochondrial function. This contributes to their reduced ability to switch between glucose- and fat oxidation if fuel availability allows to do so (e.g., after meal ingestion). The resultant hereof is an increase in blood glucose values. Glucose taken up by the muscle under the influence of insulin can either by directed towards oxidation by mitochondria, or can be stored in the muscle as glycogen.
The observed improvement in glucose uptake after training is entirely accounted for by the increased ability to use glucose as an energy source via oxidative degradation. The fraction of glucose taken up by the muscle and directed towards storage as glycogen does not improve by training in type 2 diabetic patients. For complete restoration of muscle insulin sensitivity it is hence of importance to identify routes to increase glucose storage in addition to improved glucose oxidation.
Dr Matthijs Hesselink: “Furthermore it is of relevance to note that the beneficial effects of the training program are not restricted to muscle, but also liver and adipose tissue insulin sensitivity improved significantly after training. Strikingly, these health benefits occurred without loss of body mass and did not (yet) translate into improvement in classical clinical parameters like fasting blood glucose or glycosylated haemoglobin (considered a long term reflection of glucose homeostasis). This may implicate that the health benefits of exercise training in patients with type 2 diabetes are partly masked if only the classical clinical parameters are used for evaluation of the effect of exercise programme.”
The complete title of this publication in Diabetes is: ‘Restoration of Muscle Mitochondrial Function and Metabolic Flexibility in Type 2 Diabetes by Exercise Training Is Paralleled by Increased Myocellular Fat Storage and Improved Insulin Sensitivity’. The research has been funded by a Vidi grant to Dr. Hesselink and a grant of the Dutch Diabetes Foundation (DFN) to Dr. Schrauwen.
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