The role of vitamin D in curtailing the development of obesity and comorbidities like the metabolic syndrome (MetS) and type-2 diabetes has received much attention recently. However, clinical trials have failed to conclusively demonstrate the benefits of vitamin D supplementation. In most studies, serum 25-hydroxyvitamin D (25(OH)D) decreases with increasing BMI above normal weight. These low 25(OH)D levels may also be a proxy for reduced exposure to sunlight-derived ultraviolet radiation (UVR). We have found that frequent skin exposure to a low non-burning dose of UVR reduced weight gain in C57Bl/6 male mice fed a high fat diet. Ongoing exposure to UVR also significantly suppressed glucose intolerance, insulin resistance, signs of non-alcoholic fatty-liver disease and serum levels of fasting insulin and glucose. These findings were independent of circulating 25(OH)D, and most 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 potential to prevent obesity in already ‘overweight’ mice, as well as the potential involvement of brown adipose tissue using the uncoupled protein-1 luciferase transgenic mouse (“Thermomouse”), in which thermogenesis in brown adipose tissue can be tracked in vivo. Our studies suggest that UVR (sunlight exposure) may be an effective means of suppressing the development of obesity and MetS through mechanisms that are partially dependent on nitric oxide, and other novel UVR-induced mediators.