In 2014 the global prevalence of diabetes was estimated to be 9% among adults aged over 18 years and in 2012, an estimated 1.5 million deaths were directly caused by diabetes. The WHO projects that diabetes will be the 7th leading cause of death in 2030 and considers it as one of the major global health challenges. While there are several different forms of diabetes, type 2 is worldwide the most prevalent. Type 2 diabetes is the result of an interplay between insulin resistance which is often related to environmental factors, including decreased physical activity and obesity, and insulin deficiency as a results of betacell failure, often genetically determined.
Mitochondrial dysfunction plays a role in defective insulin secretion, in insulin resistance and in the pathogenesis of specific diabetic complications. Chronic subclinical inflammation links obesity to insulin resistance and drives vascular disease associated with diabetes. Fat tissue macrophages polarize to a more pro-inflammatory phenytype by switching metabolism from oxidative phosphorylation to glycolysis. This process seems enhanced under hyperglycemic conditions. Our research focuses on the delineation of the role of inflammation in obesity-associated insulin resistance and diabetes in general and on the role of mitochondrial function in particular.