Diet and aerobic exercise are highly effective for the treatment of Type 2 diabetes, but not for obese subjects that have developed the disease when very young….
A study at the Institute for Research in Biomedicine, Barcelona, Spain, demonstrates that obese subjects between 18 and 25 years of age carry mitochondrial proteins and genes that work abnormally and that these anomalies contribute to generating insulin resistance and a reduced response to physical exercise.
Diabetes Type 2 is the most common form of diabetes worldwide and in Europe it accounts for almost 90% of the cases of this disease. “Until now, most cases were registered in subjects over 50 years of age, but young people are increasingly developing the disease,” explains Antonio Zorzano, co-author of the study and head of the Molecular Medicine program at IRB Barcelona.
Zorzano goes on to explain that the results of the clinical study are relevant for two reasons. “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.” In another study published in Diabetologia in 2009, Zorzano’s group demonstrated that morbidly obese diabetic subjects — with a body mass index over 40 — also suffer from specific mitochondrial alterations that are differentiated from classical diabetes patients.
A group of young obese adults with diabetes and another group of young obese adults without this disease followed an exercise plan four times a week for three months. The muscle biopsies of the two groups showed considerable differences in a series of mitochondrial activity proteins. “After these sessions a sedentary person shows an increase in mitochondrial proteins because the exercise increases mitochondrial biogenesis, that is to say, more mitochondria are produced,” said Zorzano. It has been demonstrated that both diet and continuous exercise stimulate greater mitochondrial activity, which in turn has a positive effect on sensitivity to insulin. In contrast, in young obese diabetic subjects some key proteins do not increase, such as the mitochondrial gene regulatory factor PGC-1α, and the protein Mitofusin-2.
“These results imply that we must classify patients with diabetes Type 2, identify the differences between the distinct phenotypes and consider specific treatments,” concludes Zorzano. The group of researchers at Trinity College Dublin, Ireland, and IRB Barcelona plan to perform a clinical study to detect more mitochondrial factors that are affected in these patients. One of the final objectives of the group is to achieve the capacity to manipulate some of the deteriorated components of young obese diabetic subjects so that they can also respond to the beneficial effects of exercise.
Hernandez-Alvarez et al. Subjects with early-onset Type 2 diabetes show defective activation of the skeletal muscle PGC-1α /mitofusin-2 regulatory pathway in response to physical activity, Diabetes Care, 2010; 33 (3): 645 DOI: 10.2337/dc09-1305