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Young Type 2 diabetics have impaired mitochondrial response to exercise
12 March 2010
MedWire News: Obese individuals who develop Type 2 diabetes early in life are unable to increase their maximal oxygen consumption (VO2max) in response to chronic exercise, which is likely to be due to mitochondrial abnormalities, say investigators.
“We are starting to observe that there are special forms of diabetes Type 2 that behave in a different way to the classical form, and these differences require specific treatments for each kind of patient,” said study author Antonio Zorzano from the University of Barcelona in Spain.
Type 2 diabetes is the most common form of the condition accounting for around 90% of all cases. It generally affects people over the age of 50 years, but early-onset Type 2 diabetes is becoming increasingly more common.
The authors previously demonstrated that young, obese individuals who develop Type 2 diabetes seem to be unable to increase their VO2max after chronic physical activity, suggesting a defective muscular mitochondrial response to exercise.
In this study, they investigated the mechanisms involved in this process further by collecting muscle biopsies from seven young people with Type 2 diabetes, aged 27 years on average, and six obese controls without diabetes, aged 22 years on average, both before and after a chronic exercise program. The mean body mass indices of the diabetics and controls were 33.23 and 37.78 kg/m2, respectively.
The exercise program lasted for 12 weeks and participants competed four 1-hour sessions per week.
At baseline, the diabetic group had 26% and 39% lower levels of the mitochondrial fusion protein Mfn2 and the α-subunit of adenosine triphosphate (ATP) synthase, respectively, than the controls. Porin expression was consistent with normal mitochondrial mass.
After chronic exercise, control participants had a 2.8-fold increase in Mfn2, plus increases in both porin and the α-subunit of ATP synthase. In diabetic individuals, although porin and the α-subunit of ATP synthase were increased after exercise, Mfn2 levels were unchanged from baseline.
In addition, levels of peroxisome proliferator–activated receptor γ coactivator (PGC)-1α were four times higher in muscle from controls following exercise, but not diabetics.
“Further mechanistic studies of these pathways in this patient group are clearly indicated,” conclude study author John Nolan (Trinity College Dublin, Ireland) and colleagues in the journal Diabetes Care.
“A more complete understanding of these mechanisms will be crucial to the design of lifestyle interventions to prevent and treat Type 2 diabetes in adolescents and young adults.”
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