Do we inherit or acquire mitochondrial dysfunction in the metabolic syndrome and Type 2 diabetes?

Abstract

The rapid increase in the incidence of Type 2 diabetes mellitus as part of the metabolic syndrome in our current societies is largely the result of an increased caloric intake in combination with a sedentary lifestyle. Mitochondria are the organelles within our body that oxidize the constituents of our food, furthermore, they provide the energy for physical activity. An imbalance between energy supply and energy consumption at the mitochondrial level may be at the basis of the current epidemics of Type 2 diabetes. This review discusses underlying pathogenic mechanisms. In particular, it will focus on the contribution of mitochondrial dysfunction in muscle and adipose tissue and the issue to what extent genetic factors are primary determinants for a mitochondrial dysfunction.

Keywords::

• adipocyte
• fatty acids
• HAART therapy
• metabolic syndrome
• mitochondria
• muscle
• thiazolidine diones
• Type 2 diabetes

Financial disclosure

The author has no relevant financial interests related to this manuscript, including employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.