There is growing concern over the escalation in obesity, and obesity related diseases such as type 2 diabetes mellitus and cardiovascular disease within the western world. The evidence thus far suggests that a combination of excessive fat intake and a reduced mitochondrial oxidative capacity, brought about through a sedentary lifestyle, leads towards lipid storage. This lipid is stored not only in adipose tissue but also within the skeletal muscle and the liver resulting in insulin resistance. Interventions that increase fat oxidation can therefore be of clinical importance when targeting such diseases. A large body of evidence exists indicating that exercise with or without weight loss can lead to improvements in both fat oxidation and insulin sensitivity with the potential to reduce the onset of type 2 diabetes mellitus. However weight loss without exercise, although it can confer improvements in insulin sensitivity, does not convey any adaptations that allow for an increase in fat oxidation. Potential mechanisms through which it is thought exercise enhances glucose tolerance and insulin sensitivity are thought to include; an increase in oxidative capacity and fat oxidation, an increase in intra muscular triglyceride accumulation, and a decrease in fatty acid intermediates such as long chain acyl-CoA's, diacylglycerol and ceramides. More recent evidence has suggested a role for the involvement of novel isoforms of protein kinase C (nPKC) in obesity associated insulin resistance.