The etiology of type 2 diabetes relates to peripheral insulin resistance and a decrease in insulin secretion. In addition, it involves multiple dietary, hormonal, biochemical, and genetic factors, many of which are associated with obesity and may reflect energy usage and metabolic efficiency. Uncoupling proteins (UCPs)  comprise a complex of several related proteins that may significantly regulate energy utilization. UCP, as a proton transporter, uncouples the proton-motive force (diminishing the proton gradient across the inner mitochondrial membrane), decreasing formation of both ATP and reactive oxygen species (ROS) with the release of chemical energy as heat. UCP2, one of 5 known human homologs (1, 2), is located on chromosome 11 (1), a site linked to lower resting metabolic rate (3). Work in model systems and in animals suggests that increased expression of UCP2 decreases glucose-stimulated insulin secretion and thus impairs glucose homeostasis and increases the risk of diabetes mellitus (4-6). In contrast, elimination of the UCP2 gene in diabetes-prone rodents decreases the risk of diabetes (7).