The role of vitamin D in curtailing the development of obesity and comorbidities like type-2 diabetes has received much attention recently. In most studies, serum 25-hydroxyvitamin D (25(OH)D) levels decrease with increasing BMI above normal weight. These low 25(OH)D levels may also be a proxy for reduced exposure to ultraviolet radiation (UVR), found in sunlight. We have found that regular skin exposure to low, non-burning doses of UVR reduced weight gain in C57Bl/6J male mice fed a high fat diet (1). Ongoing exposure to UVR significantly suppressed glucose intolerance, insulin resistance, hepatic steatosis and serum levels of fasting insulin and glucose. These findings were independent of circulating 25(OH)D, and could not be mimicked by vitamin D supplementation. We are now starting to characterize the effects of biological mediators induced by exposure to UVR, such as nitric oxide, and their efficacy in already ‘overweight’ mice (2). We are also characterising the potential for low dose UVR to activate heat production in brown adipose tissue using the uncoupled protein-1 luciferase transgenic mouse (“Thermomouse”), in which thermogenesis in brown adipose tissue can be tracked in real-time in vivo. Finally, we are comparing and combining ongoing exposure to low dose UVR with moderate physical activity. Our studies suggest that increased exposure to low dose sunlight (or phototherapy) could be included as part of a lifestyle approach to prevent and treat type-2 diabetes.