Reports had suggested that mitochondria in adipocytes may potentially have central roles in regulating substrate metabolism, energy expenditure, and the disposal of reactive oxygen species.
Interest in mitochondria had been escalating due to a recent finding that pinpointed their role in disease. Reports had suggested that mitochondria in adipocytes may potentially have central roles in regulating substrate metabolism, energy expenditure, and the disposal of reactive oxygen species (ROS).
In fact, mitochondria appeared to be involved with obesity and insulin resistance development. Obesity is often a companion to decreased insulin stimulated skeletal muscle glucose uptake (i.e., insulin resistance), which ultimately leads to type 2 diabetes and cardiometabolic disease. Altered mitochondrial physiology seems to have a role in skeletal muscle insulin resistance and metabolic inflexibility, but the exact role is highly debated.
Researchers from the Mayo Clinic in Rochester, Minnesota, teamed with information specialists in Padova, Italy, to see if they could tease out the relationship between mitochondria and obesity. Their study, published in the journal Diabetes, enrolled obese insulin-resistant women with polycystic ovary syndrome (BMI=33 kg/m2 and compared their skeletal muscle mitochondrial physiology to that of lean, insulin-sensitive women (BMI=23 kg/m2).
Maximal whole-body and mitochondrial oxygen consumption were similar between the 2 groups. However, obese women’s skeletal muscle had lower mitochondrial coupling, diminished phosphorylation efficiency, and elevated mitochondrial H­2O2 emissions compared to lean women. These measures indicated mitochondrial dysfunction.
Next, participants engaged in 12 weeks of aerobic exercise, consisting of 60 minutes of stationary cycling at a heart rate corresponding to 65% of VO2 peak, 5 days per week. They examined obesity-related insulin sensitivity impairments and mitochondrial energetics on an empty stomach and following a high-fat, mixed meal.
Exercise training reversed obesity-related mitochondrial derangements. Mitochondrial bioenergetics efficiency improved and H­2O2 emissions fell. Exercise training increased catalase antioxidant activity and decreased DNA oxidative damage, the mechanism by which the researchers suspect insulin sensitivity improved.
At the study’s start, H­2O2 emissions were refractory to a high-fat meal. After 12 weeks of aerobic exercise, H­2O2 emissions were responsive (increased) following the meal, which was similar to the findings in lean individuals.
The researchers concluded that exercise effectively appeared to restore mitochondrial physiology toward that of lean, insulin-sensitive individuals.